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What is the exact principle of capillary isotachophoresis?
I know it's a type of capillary electrophoresis, but I don't get how does the separation happen exactly.

Many of us are using isotachophoresis all the time without even realising it. The explanation that follows may not be exact, but I hope that it helps.
Firstly, think about a simple electrophoresis set-up - in agarose electrophoresis of DNA we have a uniformly distributed buffer such as Tris-borate. The current is carried by the borate ions and the DNA molecules run through the homogeneous electric field towards the anode. They separate by size because of the sieving effect of the agarose matrix.
Now let's think about what is happening in an SDS-PAGE separation (a Laemmli gel). Just to remind you:
The running (or reservoir)  buffer is Tris-glycine pH 8.3
The stacking gel is in Tris.HCl pH 6.8
The separating gel is in Tris.HCl pH 8.8
When the power supply is turned on, the glycinate ion in the top reservoir begins to move into the stacking gel. When it hits the zone of pH = 6.8 it is much closer to its pKa and so is now only weakly charged. Consequently it slows down. Meanwhile the chloride ions in the stacking gel have begun to move rapidly down through the stacking gel (towards the anode). This creates a discontinuous electric field: the chloride zone has a lower resistance than the glycinate zone so the field strength in the chloride zone is weaker than the field strength in the glycinate zone. This is a stable situation because the ions cannot stray into each other's zones: if a glycinate ion happens to diffuse forwards into the chloride zone it will experience a weaker field and slow down, whereas if a chloride ion diffuses back into the glycinate zone it will hit the stronger field and quickly move ahead again.
What about the SDS-protein complexes that were in the well? (I'll just refer to these as proteins from now on.) Their ionic properties lie between the glycinate and the chloride, and so they eventually end up moving through the stacking gel between the trailing zone of glycinate and the leading zone of chloride. Any protein that finds itself in the glycinate zone will move quickly forward (due to the higher field strength) and any protein that moves ahead by chance into the chloride zone will slow down due to the weak field strength, falling back into the protein zone. And in this way these zones move in a procession through the stacking gel, with the proteins being focussed into a very narrow region in the middle. The glycinate, the proteins and the chloride are all moving at the same speed, and so this is an example of isotachophoresis (isotacho- = "same speed"). The polyacrylamide gel matrix in the stacking gel has no separating function - its role is simply to stabilise against convective effects. The proteins can reach very high local concentrations in the stacking gel, and if you look carefully you will often see refractive effects as your sample runs through the stacking gel. In this way the protein sample is "applied" to the separating gel in a very tight band, perfect for achieving high resolution separation (bands broaden by diffusion in the separating gel so the tighter the bands ar eat the point of loading, the better the final result.)
Once the sample hits the separating gel, all of this breaks down: the pH is now 8.8 so the glycinate becomes strongly charged and zooms off ahead with the chloride through the gel, leaving the proteins to move more slowly due to the sieving effect of the polyacrylamide matrix.
It is possible to set up an isotachophoresis as described above in isolation. Individual proteins will have slightly different ionic properties and will line up in the region between the two buffer ions, allowing for their separation.


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How do individual plants adapt to changes in temperature?
If you grow a plant from seed in your nice warm house, then plant it out in your temperate garden, it will stop growing for a while, possibly die, and if not, subsequently resume growth. Standard gardening practice is to 'harden off' plants, moving them to an area of intermediate temperature for a while before planting them out.
Why does this happen? What is the difference between a plant adapted to a warm environment and one adapted to a cold environment?
Expression of cold-tolerance genes? Levels of some secondary metabolite? Thickness of cell walls? Density of root hairs?
An unidentified author on the Royal Horticultural Society website states that
"The effect of hardening off is to thicken and alter the plant's leaf structure and increase leaf waxiness", which is not quite detailed enough to satisfy.

Cf. Why are some plants frost tender

As far as I know, the main challenges the plants have to face in cold environment are metabolism reduction and membrane fluidity. If the temperature is even lower, they may face freezing.
Increasing the metabolism is quite hard, because plants usually are unable to increase their temperature by its own. Plant may produce more pigments in order to absorb more sunlight; grow trichomes and other structures that may generate an air layer which acts as an insulator or simply reduce its metabolism by, for instance, hibernation. The amount of stomata is also related to temperature, and a plant growing in low temperature needs less stomata.
In bacteria sometimes there exist isoforms of many enzymes that are expressed during different conditions, and since plants usually have large genomes with tons of duplications, it's reasonable that some plants may express different genes for the same processes in high and in low temperature. One group of genes that are certainly expressed in cold exposition are membrane desaturases, which introduce unsaturation in the lipids, increasing the fluidity of the membranes. Some plants also protect themselves of freezing by accumulation of some substances, such as glycerol or proline, avoiding the formation of ice inside the cells.

Miguel Angel Naranjo Oritz Excellent answer. Could you provide a source for your information that plants hibernate ?

In botany the term hibernation, or winter dormancy (as opposite of estivation, wich is the same for summer months) describes the reduction of metabolism during winter. The most obvious example are trees that lose their leaves during the fall. Maybe I used a term a bit confusing.

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Are chromosomes from each parent split between gametes with equal probability (esp. in humans)?
I've recently read a little on Wikipedia about genetics, but I can't find a direct answer to this question.
My rough understanding is this:

Both males and females have pairs of chromosomes, one copy from each parent
Both produce gametes (eggs in females, sperm in males)
The gamete is produced during something called 'meiosis' to take only one set of genes

What I can't find an answer to though is whether that selection is completely random, such that every chromosome in a gamete has an equally likely chance of being taken from the male parent set and the female parent set.
Another way of putting it, perhaps: Would the range of 100% male parent to 100% female parent chromosome selection in the gamete be a binomial distribution?
My background is computing, so please assume very little knowledge of biology.

To clarify on your question: Imagine a species with two pairs of chromosomes, with one member of each pair coming from each parent. So there is one copy of chromosome 1 from the father (1F) and one from the mother (1M) and the same for chromosome 2 (2M and 2F) with one member of each pair going in to a gamete. Do you want to know whether the 1M+2M or 1F+2F combinations would be more common in the gametes than the 1M+2F or 1F+2M combinations?

Not quite - what I want to know is whether nM is just as likely to be in the gamete as nF. Another way of putting it (maybe): Is it correct to say (in a human for instance) that a gamete has a 1 in 2^23 (~1 in 8 million) chance of having entirely the nM or nF set of chromosomes? Also, in that extreme case, would such a gamete be indistinguishable from a gamete from the parent? Say, a male producing a sperm with 23 chromosomes all from the male parent.

I have heard of some research being done in to whether the chromosomes associate in such a way but can't remember who was doing it, also you might want to look at meiotic drive elements. However recombination occurs between chromosomes so the chromosome in a gamete is also likely to be a cocktail of the parental ones - here is a wiki section that should help, I might write an answer this weekend for you http://en.wikipedia.org/wiki/Intragenomic_conflict#Nuclear_genes

Other answers are correct in their own terms, but because of homologous recombination during meiosis, the idea of maternal and paternal chromosomes becomes meaningless. Any chromosome in a gamete will be a mosaic of the maternal and paternal versions. In this sense the chromosome is not the unit of inheritance.

Ah.... that's really helpful, I didn't realise the chromosomes themselves were mixed up like that.

Have marked as the answer - but one other question in relation to this, if I may. This 'mosaic', what would be the 'unit' of this? Is it at the gene level? So a resulting chromosome would be a mixture of genes from each parent chromosome pair?

@MarcosScriven no it is not at the gene level, it is usually in a much larger scale than that, resulting in the mix of groups of genes. This is a process that has nothing to do with genes really, if genes are the paragraphs in a book, meiotic recombination consists of mixing up the pages. This means that genes can be split as well.

As far as we know, chromosomes tend to be equally distributed across normal gameteogenesis, following Mendel's second law of independent assortment. However some versions of DNA repair and chromosomal condensation can malfunction and result in more versions of one parents genes in a cell than another. Two phenomena which are exceptions to the equal parental ratio are Gene Conversion and Chromosomal Fusions.
Although a much smaller scale than chromosome segregation, Gene Conversion is a case of unequal allele transmission. While repairing double strand breaks during meiosis, one parent's DNA may be used as the repair template instead of the original version. This phenomena distorts the 1:1 allele ratio on the scale of hundreds of base pairs.
Robertson translocations are when two nonhomologous chromosomes fuse into one. Chromosomes which were once separate, segregate together into the same gamete. These cases can serve as exceptions to Mendel's second law of independent assortment.
There are also several cases of transmission distortion, while these cases may not affect the segregation of chromosomes during meiosis, they do cause unequal fertilization. The t-haplotype in male house mice, is passed on to up to 95% of offspring! The mechanism is still under investigation, but it appears that this gene when expressed in sperm, kills all other sperm without the t gene. The Sd gene is a similar element in Drosophila.
A great book on selfish genetic elements and intragenomic conflict is Genes in Conflict by Burt and Trivers.

Yes, every chromosome in gamete has an equal probability of being taken from the male parent set and the female set.

Thanks for answer. While I'm here is there a technical term for 'male parent chromosome set'?

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What is meant by “global RNA polymerase occupancy”?
I read the following in a paper

It provides base-pair resolution and strand-specific information of **global RNA polymerase** occupancy.
CDK13 cooperates with CDK12 to control global RNA polymerase II processivity

What does this mean?

Please provide a reference to the article/textbook you are citing.

"Global" tends to be used in contrast to "local". I think you need to read the paper to find out more specifically.

it looks like you are posting quotes without acknowledging them as as such or noting where they come from. It would help for you to clearly restate a more expansive version of your question outside of the title for us to be able to help more effectively.

In context of the PRO-seq method, "global" can be substituted for "genome-wide". Note that use of the term global is a call-back to the methodological predecessor of PRO-seq, which was called global run-on sequencing (GRO-seq).

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Why were there relatively fewer papers about cell fusion before the 1950s?
While working on my cell fusion technology report, I saw PubMed's cell fusion graph of results by year. There have been studies or research since the early 1900s, but until the 1950s, there were no more than ten papers. But, after the 50s, scientists studied a lot of cell fusion. I wanted to know why this happened, but I could not find any reasons on the internet. So, I ended up coming here.
I searched in Nature, PubMed, and google, but there was no detailed explanation of it.

Since you need to be able to grow cells for studying their interactions, I think the main reason for this is the development of cell culture techniques in the late 1940s and early 1950s. As an example of one of the earliest (cancer) cells in culture we can name the HeLa cell line, which was established from a cervical cancer in 1951.
There have been earlier attempts to grow pieces of tissues which at least have been partially successful, but for immortal cell lines attempts failed. See the references for an overview.
With the rise of cell culture in the 1950s, it was possible to reliably grow the cells needed for vaccine development, monoclonal antibodies and also cell-cell interactions.
The figure with the timeline comes from reference 2:

References

A History of Cell Culture
History of Cell Culture

I wouldn't underestimate the effect of public interest sparked by Watson & Crick's characterisation of the structure of DNA in '53 too.

@JiminyCricket. Interest in Biology was high at that time - even famous theoretical physicists as Max Delbrück changed over to molecular biology and genetics.

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Desplasmolysis while maintaining hypertonicity
I prepared a sample of an onion cell by putting it in a hypertonic solution and was able to observe plasmolysis. However, when I observed it few hours later using a microscope, I found that deplasmolysis had occurred and the cells had returned to normal (not completely but appreciably). How can this be explained?

Welcome to SE Biology. Please do us the courtesy of finishing reading the [Tour] to find out how this site works, and especially the Help section on writing a good question. I have edited your title as an example because the English was unacceptable. However I think it unlikely that anyone can do more than guess at the cause of your problem, if the outcome is contrary to expectation.


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How to model the relationship between environments based on environmental covariates in a genomic prediction context
I have a dataset with different wheat lines in multiple environments. For each line various traits are measured (e.g. grain yield). I am trying to set up various genomic prediction models (linear mixed models) in order to predict these phenotypical traits based on the plant genomes, as well as the environment in which they are growing.
For the different environment, various environmental covariates (EC) were measured, like precipitation, temperature, etc. I would like to incorporate these covariates into the prediction models by creating a covariance matrix that represents the similarity between the different environments based on the different covariates. This would allow for the borrowing of information between the environments and genotype lines, when used in combination with a G-matrix.
This is based on a paper by Jaquin et al. (2014): https://doi.org/10.1007/s00122-013-2243-1
(See page 4: Extending G‑BLUP with addition of environmental covariates)

Consequently, the vector w = Wγ follows a multivariate normal density with null mean and a
(2) yijk = µ + Ei + gj + εijk
covariance matrix proportional to omega whose entries are computed as those of the G-matrix but using ECs instead of
markers. This covariance structure describes the similarity
between environmental conditions in a similar way that G
describes genetic similarity between lines.

Here they mention that they compute the environmental covariance structure in the same way as the G-matrix. But I'm unsure how this is done, because the covariates are continuous and not frequencies or count data. What would be a feasible way to go about this? Or would it be better to just compute a 'normal' similarity matrix that is based on the euclidean distance for example?

Can you look into how they compute the G matrix and add that information here? Is there a mathematical or procedural reason why continuous data cannot be used in the construction of a G-like matrix for environmental covariates? It would be good to separate in your question the concerns of whether you can do it and whether it is a good idea. I expect that the first question is very answerable with a little work, the second question may be very difficult to answer without a lot of expertise/reading.


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What is the big plant with white flowers on the photo?
What is the 3m tall plant with white flower? It is from Central Europe and there is a creek near to it. I have a guess, but I want to know for sure...

Is the small one the same species?

More high res photos here:

https://ibb.co/cAaUMU
https://ibb.co/ih4Zo9
https://ibb.co/eJSyFp
https://ibb.co/gstS89
https://ibb.co/kQ2OWU

Probably Angelica sylvestris. (No time to look more closely now)

The small one looks like Ground Elder (Aegopodium podagraria)... Were the leaves serrated?

@JulPal I think so. But they looked like the big plant, which was 2.5m tall...

The photos are high res, but out of focus and motion blurred so it is really hard to identify accurately.

Most of the links don’t work and the photos are still rather blurry however the plant in question appears to be Angelica sylvestris, wild Angelica. I am extremely disappointed with previous answers proclaiming it ground elder or poison hemlock; ground elder has elder like leaves, hence the name and poison hemlock has finely divided, carrot like leaves!!!
A height of 3 meters would be quite exceptional for wild Angelica; are you sure you have measured it correctly?
In the bottom image there is also a Heracleum spondylium, common hogweed plant, as well as a hedera spp ivy growing near the Angelica, both of which also vaguely similar blooms though I see no blooms on the ivy!

The plant could also be Cicuta virosa but the well defined leaflets and umbel shape make me lean towards Angelica

https://commons.wikimedia.org/wiki/File:Illustration_Aegopodium_podagraria0_clean_no-description.jpg

They both look like poison hemlock (Conium maculatum).  It can grow up to 3m tall and grows in moist areas including along creekbeds. One of it's common names is European Hemlock.  It is toxic to some domestic animals and humans.

Source: United States Department of Agriculture

Source: http://natureid.blogspot.com/2011/11/poison-hemlock-111211-elkhorn-slough.html

According to wiki it can grow only 2m tall. I checked other photos, the flowers are smaller and not that dense. I thought first it is https://en.wikipedia.org/wiki/Heracleum_mantegazzianum but the leaves are different. It is in the https://en.wikipedia.org/wiki/Apiaceae family and I suspect I had phototoxicity from it on my leg, but I am not sure. It might be unrelated.

The closest I could find based on the leaves is Angelica atropurpurea . No idea what it does in Europe though, it should be in America. :D

I concur, not Conium maculatum the overall habit is completely different.  Also, if you just took these photos and are not at particularly high altitude C. maculatum should have finished blooming (it has finished at least a few weeks ago in the Central US).  C. maculatum has a distinct mousey smell which is hard to miss, and it very toxic to the point it should not be handled with bare hands.

@inf3rno if you had touched H. mantegazzianum, you would have known, trust me. I slightly touched it with the rear of my knees and after a couple of hours I couldn't bend them without almost screaming in pain. It is not a pain you cannot be sure of.

@inf3rno: Huh, according to the USDA it can grow to 3m tall - maybe that's just in the US.  I'm glad it wasn't Giant Hogweed (H. mantegazzianum).  I've never touched it as LinuxBlanket has but we were given a flyer at work earlier this year warning us about it

@LinuxBlanket Well then I was lucky with my plant. I had only rash and now 1 week after it some small red blisters. I used sunscreen on it, I am not sure whether it was phototoxicity or my skin was red because of other kind of toxicity. I am not even sure what I touched, I started to look for toxic plants only after I had the rash and I found this. I am pretty sure it is some kind of Angelica, but there are so many species... :-)

@Linuxblanket Reaction to H. mantaggazianum varies greatly between people and depends strongly on exposure to the sun.


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Animal swimming styles
Can a frog swim on its back, or it can use only the classic frog style? Does any (not specifically marine) animal exist with many different swimming styles, just like humans?

Don't know whether it was ever investigated, but I'm pretty sure, that frogs can in principle swim upside down (e.g. when escaping from predator), but they normally do not do it.
One example of alternative swimming styles in animals is provided by some munnopsidid isopod crustaceans. Several genera are pelagic and have very elongated forelegs equipped with rows of setae and paddle-like hindlegs (see Marshall & Diebel 1995 and Giver 1998):

the forelegs are used to "walk" in the water column
the same legs can be stretched out for passive parachuting
the hindlegs are used for backward swimming

Below is a photo of a parachuting specimen. And here is a very nice video of a backward swimming specimen.

Foto by Karen Osborn from here

Does this count swimming? https://www.youtube.com/watch?v=45yabrnryXk :D

Yes, creatures can swim different ways.
If you drop a frog into water while it is in the ventral up position, it will indeed swim upside down to escape before righting itself, which occurs by rotating while swimming. If the water is too shallow, it will flop and flip before jumping away.
Swimming on the surface ventral side up is kind of silly for a frog since it's eyes would be looking into the water, and it wouldn't see predators or prey on the surface. But I doubt if it is impossible. It's certainly not instinctual. To see an aquatic animal belly-up usually means something bad.
Otters can float belly up and even swim that way:

While snorkeling, I have seen many fish (especially parrot fish) swimming completely sideways in order to keep an eye on me while I hover over them.
Male orcas will swim upside down to mate, and will float upside down when semen is collected. Cetaceans have been taught to swim on their sides and expose one flipper to give the appearance of waving. In the documentary Blackfish, you can see Tilicum doing just this thing, circling the enclosure on his side waving for two or three laps before killing one of his trainers. Other orca videos show Tilicum swimming upside down to show off their white ventral surface for the crowd. And dolphins, of course, can swim backwards.
Dogs will do the dog paddle on the surface of the water, but use a slightly different swimming technique to dive.

I wish I could provide videos but I can't find them.

Yepp, it is pretty hard to find videos. :S Thank you for the answer!


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Rosemary room temperature at winter
I consistently read in non-scientific resources that I have to put my rosemary to low temperature (about 10°C) in winter (unless I don't want it to freeze). I googled, but I fail to find a scientific resource about why room temperature is not good for it. Do you have any explanation (with scientific references ofc.)?

can you provide any reference to the article where you got the info?...cause your q is not too clear...like, in winter you want to keep the plant in low temperature, in order not to freeze it....it's ridiculous...

@souvikbhattacharya It doesn't freeze by 10°C, which is lower than standard room temperature 20°C. What don't you understand?

Either the rosemary is a naturally cold-weather plant and just prefers colder temperatures, or the plant needs cold weather to trigger winter behavior. Some plants need to hibernate during the cold months.

@JeremyKemball What if I don't trigger the winter behavior? Ohh actually that is the main question as well...

I have no idea. You might be able to find someone who knows a lot about rosemary on gardening.stackexchange.com ? The tree equivalent is called vernalization and can apparently out and out kill a tree. I have no idea why, but there you go.

@JeremyKemball Do you think this is off-topic and should be moved to gardening?

I mean you'd have to reword it to something more like 'what happens if I don't properly overwinter my rosemary' but this isn't entirely off-topic here. It might be unanswerable due to lack of research, but on-topic nonetheless.

@JeremyKemball I created a topic in gardening as well. The result is unconclusive yet. Some of them claims that it would survive in room temperature, some of them claims the opposite. :-) I'll try to find articles about mediterran plant hibernation meanwhile.

I did not find scientific articles in the topic. Non scientific resources claim that is is possible to overwinter rosemary at room temperature, but it is hard. It requires at least 8 hours of light, humidity, and almost, but not totally dry soil. I'll give it a try.

As a bioassay, I have for years seen rosemary growing in the median strips of highways in Downtown Las Vegas, a pretty warm place most of the time. You can Google Vegas weather data, but it has to be well over 100 F in those medians much of the year. Right next to Bellagio they had rosemary growing in the medians for years, not sure if it is still there.

@LynnGriffith I asked a botanist. According to her, it can withstand -15°C degrees, so I left it outside. It's still alive! :-)


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From STRUCTURE to FSTAT format
From numerical simulations I output a file that is input to STRUCTURE (Hubisz et al. 2009). I now realize that I would need to process my data with FSTAT (Goudet 1995). Both are text files.
Is there an extant algorithm that would reformat a file that is input to STRUCTURE into a .fstat format?

What kind of files are these? If they are text files then reformatting would be easy; in that case this question would be off topic.

Yes these are .txt files. My question is very specific to data format used in bioinformatics though and I am not asking for help to build my own algorithm to reformat but am asking for extant algorithm that would do the job. Does it make my question off-topic?

PGDSpider will do the trick.
PGDSpider is able to parse 31 and to write 35 different file formats including STRUCTURE and .fstat.


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Why add hydrogens in molecular dynamics simulations?
In my molecular dynamics lecture, our prof said, that we always have to add hydrogen atoms to titratable groups, before we start the force field simulations, and that it is especially important for Histidine.
But why is that? Why do we always have to add the hydrogen atoms? And do we only have to do that for titratable groups, or for all?

I refer to this presentation: https://www.mpibpc.mpg.de/15151147/Lecture3_JH_20151117.pdf (On the second slide on the bottom)

Ok, and why do we only have to do that for the titratable groups?

The RCSB Protein Data Bank (PDB) presently has 137,917 structures deposited in it, of which less than 10% have been solved by nuclear magnetic resonance (NMR). Most techniques in structural biology simply cannot resolve the positions of hydrogens in macromolecular structures; only NMR and neutron diffraction provide the positions of hydrogens "by default." Therefore, all-atom molecular dynamics force fields, the most notable of which are the OPLS, CHARMM, and AMBER series, require that the positions of hydrogens be deduced from the starting macromolecular structures and geometric criteria and patterns, that hydrogen bonds are known to generally follow, if the starting structure doesn't have hydrogens. "Generally" is an important word to point out here, as there often is no unique, unambiguous way to place the hydrogens in a structure. This is especially true of histidine, where the local environment of residues and/or cofactors may perturb its pKa in often unexpected ways. Simulating histidine in the wrong protonation state, when that histidine is an active site and crucial to the mechanism and process under study, may lead to spurious, misleading, and/or potentially nonsensical results. Hydrogens are required for a faithful, (relatively) realistic description of macromolecular structure, simply because they are always present in macromolecules and are crucial for macromolecular structure and functioning - recall that hydrogen bonds stabilize the secondary structure of proteins, the DNA double helix, etc., moreover, they often mediate intermacromolecular recognition and function. Thus, an explicit representation of hydrogens is required. The so-called coarse grained force fields, the most popular of which I believe are the various versions of MARTINI, group hydrogens along with heavier atoms to achieve an increase in the simulation time step and to reduce the number of particles in the system, but these force fields are a very poor choice when modeling specific recognition and interactions.
The ambiguities of protonation are not a matter of opinion, I'm afraid. One can go through all the structures in the PDB, only to find that the majority of  them have no hydrogens at all. One can explore the link to the PDB I've provided; one will find that out of the 131,917 structures in the PDB, 123,461 have been resolved by X-ray crystallography, of which only 10,749 have a resolution below 1.5 Å. To resolve hydrogens, a resolution below 1 Å is required. Indeed, high resolution crystal structures, NMR structures, and neutron diffraction structures (only 60 in the entire PDB!) are less than 20% of the entire structural archive. Techniques like electron microscopy have resolutions between 4 and 10 Å; in such cases, people are unsure about the positions of the heavy atoms; they don't even dare think about the hydrogens. So, it's not just the titratable groups that are problematic, in most structures one can't see ANY hydrogens. Of course, for backbones and alanine side chains, one probably has a pretty good guess where the hydrogens are, given the positions of the heavy atoms. But to answer the question - in MD, most often one needs to add hydrogens everywhere, not just in the titratable groups, because the starting PDB structure doesn't have any hydrogens. In fact, often times structures from the PDB have missing heavy backbone or side chain atoms, because those couldn't be resolved; sometimes termini are missing, sometimes large stretches of protein; these often need to be modeled-in.

@xusr, please see the edit to my answer, it was too long to post as a comment.

Your statement that "only NMR provides the positions of hydrogens by default" is not true. Neutron diffraction also indicates positions of hydrogen atoms (precisely enough to be able to assign orientations of organized water molecules!).

Thank you for your comment @Guillaume, I will edit my answer accordingly.


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Why is a heritability coefficient not an index of how "genetic" something is?
On his blog, Eric Turkheimer writes:

[T]aken as a number, a unit of analysis, heritability coefficients are
  funny things to aggregate on such a massive level.  What exactly are
  we supposed to make of the fact that twins studies in the
  ophthalmology domain produced the highest heritabilities?  Should eye
  doctors, as opposed to say dermatologists, be rushing to the genetics
  lab because their trait turns out to be more heritable?  No.  Whatever
  else a heritability may be, it is not an index of how "genetic"
  something is.  It is not, for example, a useful indicator of how
  successful gene-finding efforts are likely to be.  If nothing else,
  differences in reliability of measurement are confounded every
  heritability tallied here.  My point is this-- although it's nice to
  know that on average everything is 50% heritable, it's hard to attach
  much meaning to the number itself, or especially to deviations from
  that number, to the fact that eye conditions have heritabilities
  around .7 and attitudes around .3.  Having two arms has a heritability
  of 0.

As I understand this, one reason Turkheimer believes heritability coefficients are not an index of how genetic a trait is is that they are confounded by varying levels of measurement error. So, for example, maybe the relatively low heritabilities in skin conditions compared to eye conditions are because there is more measurement error in relation to skin conditions.
Turkheimer implies that there are other reasons why it's not appropriate to say a heritability coefficient is an index of "how genetic" something is. What are those other reasons?

Heritability is indeed an index of how genetic something is; it is just that there are useful caveats (mentioned in the answers). That "something" is "a phenotype within a specific population in a specific environment at a specific point in time," not just "a phenotype."

Rather than discussing what heritability is not through wordy sentences, let's just talk about what heritability is. There are two "types of heritability":

Heritability in the broad sense
Heritability in the narrow sense.

I will discuss a few concepts and slowly introduce the concept of heritability in both senses.
Phenotypic trait
The phenotype is the consequence of the genotype on the world. In brief, a phenotypic trait is any trait that an individual is made of!
Quantitative trait
A quantitative trait is any trait that you can measure and ordinate, that is any trait that you can measure with numbers. For example, height is a quantitative trait as you can say that individual A is taller than individual B which is itself taller that individual C.
Variance of a quantitative trait
In a population, different individuals can have different values for a given phenotypic trait $x$. Because we are talking about quantitative traits we can calculate the variance of the trait in the population. Let's call this variance $V_P$ such as
$$V_P=\frac{1}{N}\sum_i (x_i - \bar x)^2$$
In the above equation, $x_i$ is the value of the phenotypic trait $x$ of individual $i$. $N$ is the population size (there are $N$ individuals in the population) and $\bar x$ is the average phenotypic trait $x$ in the population.
$$\bar x = \frac{1}{N}\sum_i x_i$$
What is causing phenotypic variance
Why would a population display any phenotypic variance? Why wouldn't we just look exactly the same? What explains these differences?
For some traits, we see very little variance. To consider the example the OP gave in the post, the number of arms in the human population shows very little variance. However, there is quite a bit of variance in terms of the number of IQ, in terms of height or of weight.
There are two (main) sources of variance that are underlying this phenotypic variance. The first one is the genetic variance and the second one is the environmental variance. We will call the genetic variance $V_G$ and the environment variance $V_E$.
If in a population, people vary a lot in terms of how many hamburgers they eat, then there is a non-negligible $V_E$ underlying the phenotypic variance $V_P$ for weight. If in a population, there is a lot of variation of genes affecting weight, then there is a non-negligible $V_G$ underlying the phenotypic variance $V_P$ for weight.
By the way, a gene (or another non-coding sequence) that is polymorphic (i.e. has more than 1 allele in the population) and which explains some of the variance in the phenotypic quantitative trait is called a Quantitative Trait Locus (QTL). A locus is a sequence (of any length) on the genome.
Math reminder
Variances of uncorrelated variables can simply be added! For simplicity, we will assume for the moment that we are considering uncorrelated variables. As a consequence, we can express the phenotypic variance $V_P$ as a sum of the phenotypic variance that is due to environmental variance $V_E$ and the phenotypic variance that is due to genetic variance $V_G$
$$V_P=V_E+V_G$$
This equation is slightly simplified and this will affect the below calculations. See the section Other sources of phenotypic variance for more info.
We can now talk about heritability!
Heritability in the broad sense
Heritability in the broad sense $h_B$ is defined as the fraction of phenotypic variance $V_P$ that is explained by genetic variance $V_G$. In the equation, it gives:
$$h_B=\frac{V_G}{V_P} = \frac{V_G}{V_E+V_G}$$
Heritability in the narrow sense
Heritability in the narrow sense $h_N$ makes one further trick. We have to consider that the genetic variance $V_G$ that is underlying the phenotypic variance can itself be decomposed into a sum of variances. The variances that we like to consider the additive genetic variance $V_{G,A}$ and the dominance genetic variance $V_{G,D}$.
The additive genetic variance is the genetic variance that is due to additive interaction between alleles. The dominance of genetic variance is due to non-additive interactions between allele.
We can now define the heritability in the narrow sense $h_N$ as the is defined as the fraction of phenotypic variance $V_P$ that is explained by the additive genetic variance $V_{G,A}$. In the equation, it gives:
$$h_N=\frac{V_{G,A}}{V_P} = \frac{V_{G,A}}{V_E+V_G} = \frac{V_{G,A}}{V_E+V_{G,A}+V_{G,D}}$$
In the special case, when all the genetic variance $V_G$ is exclusively done through additive interactions, then $V_{G,D} = 0$ and $V_{G,A}=V_G$ and therefore $h_N=h_B$
Interpretation of the heritability
If all of the phenotypic variance is due to genetic causes (and regardless of whether there is a lot or a little variance), then $h_B=1$. If all of the phenotypic variance is due to environmental variance, then $h_B=0$.
So what does a $h_B=0.3$ means?
It means that 30% of the phenotypic variance is explained by genetic variance and that 70% of the phenotypic variance is due to environmental variance.
So, what if there is no phenotypic variance in the population? if $V_P=0$, then the heritability is undefined (as dividing by zero is undefined). However, in general, we tend to think that there is always a tiny bit of environmental variance and most people would just go on saying that heritability is 0 when $V_P=0$.
What will affect the heritability?
A measure of heritability is true for one population, in one environment.
If you change the population, add a few mutations for example, you might well create a polymorphic locus that is causing some phenotypic variance. If you put the same population in another environment, you could suddenly have more or less phenotypic variation due to environmental variance. Typically, if you measure heritability in the lab in a controlled and constant environment, then you will likely overestimate the heritability (as you underestimate $V_e$) compared to the same population that is living in a very heterogeneous environment.
What heritability is not!
If a trait has low heritability, it does NOT mean that it is (or is not) an adaptation. It only means that there is no genetic variance that explains the phenotypic variance.
Why do we care about heritability?
If there is no genetic variance for a trait, it means that the only way this trait can change through time is by changing the environment (or by creating a non-zero genetic variance through mutations). If there is a non-zero genetic variance and if there is a difference in fitness between individuals having different trait value then, the trait is under natural selection.
The most commonly used index of heritability in the heritability in the narrow sense $h_N. $Why do we care about $h_N$?
Let $\bar x_t$ be the mean phenotypic value of the trait $x$ at time $t$. One generation later, that is at time $t+1$, the mean phenotypic value is $\bar x_{t+1}$. Let's define the response of selection $R$ as the expected difference between these two quantities, that $R=E[\bar x_{t+1} - \bar x_t]$. Let's define the strength of selection $S$ and the heritability in the narrow sense $h_N$, then
$$R=h_N \cdot S$$
As a consequence knowing $h_N$ allows us to predict the effect of selection on a given trait.
This equation is called the breeder's equation (see this post about its interpretation).
Other sources of phenotypic variance
Saying $V_P=V_G+V_E$ is a little too simplistic. In reality, there are other sources of phenotypic variation such as variance due to epigenetic changes $V_I$ and variance due to developmental noise $V_{DN}$ for example. It is also sometimes very important to consider the covariance between any pair of such variance. So, the equation would more correct if stated as
$$V_P = V_G + V_E + V_I + V_{DN} + COV(V_G, V_E) + COV(V_G, V_I) + COV(V_G, V_{DN}) + COV(V_E, V_I) + COV(V_E, V_{DN}) + COV(V_I, V_{DN})$$
Note that everyone is free to further decompose any of the above variance into a sum of variances as we did above for the genetic variance. For example, the environmental variance $V_E$ could be decomposed into the sum of the phenotypic variance due to variance in temperature $V_T$ and the phenotypic variance due to variance in precipitation $V_{\text{precipitation}}$ assuming the other types of environmental variances are negligible.

It is an wonderfully thorough answer! Is it fair to say that if $h_B=0$ there is definitely no point looking for a gene that causes the variation in the trait, because the variation has nothing to do with genetics?

@user1205901 Yes a comment has been deleted. We can now delete all the extra comments. Thanks

@user1205901 Exactly. As you said if $h_B=0$, then none of the phenotypic variance is due to genetic variance. In other words, there exists no gene which is currently polymorphic and which polymorphism affect phenotypic variance in the population in this environment. I added two small paragraphs to try to troubleshoot potential misconceptions about heritability.

So, if $h_B=0$ then there is no point looking for polymorphic genes that affect the trait. Turkheimer says that heritability coefficients are "not...a useful indicator of how successful gene-finding efforts are likely to be". However, isn't it the case that the heritability statistic is somewhat useful in telling us whether to devote efforts to gene-finding? If $h_B=0$ we are definitely wasting our time on gene-finding efforts, if $h_B=0.00001$ we are most likely wasting our time, whereas if $h_B=0.9999$ gene-finding efforts are more likely to be successful?

If $h_B=0$, then you are definitely wasting your time in trying to find genes which variance in the population affect the phenotypic variance in the population because there are none. But if $h_B≠0$, then there are such genes (or other non-coding sequence). All else being equal (typically the number of genes that affect the trait (which are called QTL btw)), the higher the heritability the smaller the sample size you will need to find the QTL.

Note again that when $h_B=0$, you might still be interesting in the genes that are involved into the building of the trait even if these genes are not polymorphic.

@remi.b sorry I removed my comment, I think it generated confusion, I have added another answer, and use the aforementioned Y chromosome work at the end to illustrate

ps @Remi.b I'm curious - why do you use the notation $h_B$, $h_N$, $V_{G,A}$, $V_{G,D}$... ? It's very unusual for me (I'm used to using $H^2$, $h^2$, $V_A$, $V_D$... respectively) - (that's not to say I think you are wrong to use them of course, it's just variants I've not seen [much] before)

I never saw $V_{G,A}$ and $V_{G,D}$ either but I just thought it would highlight the fact they are components of $V_G$. However, I am used to $h_B$ and $h_N$ at least in discussions and conferences. I am not used to $H^2$ and $h^2$.

I'm not a Biology person, but variances are not additive. From what I read on Wiki, these variances are or can be additive. In general, variances are not additive.

@BCLC Given 3 variables A,B, and C. If C = A + B, then var(A) + var(B) = var(C) if A and B are independent. Am I right? I said that the equation was a simplification (in the sense that it assumes independence). I now added some more info to avoid the confusion.

@Remi.b If independent. Too strong though you can just say uncorrelated. I think I read on wiki that uncorrelated is good enough here

Heritability is not a measure of how genetic a trait is. It's a measure of how much of the variation in the trait is due to variation in genetics.
I'll try to make this clear with a story, to supplement the answers that rely more heavily on mathematics.

For reference: technically it's the fraction of phenotypic variance
  which is due to variance in genetic effects: $H^2=\frac{V_G}{V_P}$ (if
  you're talking about heritability in the broad sense); or, it's the
  fraction of phenotypic variance which is due to variance in
  breeding values: $h^2 = \frac{V_A}{V_P}$ (if you're talking about heritability in the narrow sense). $V_A$ is also often called
  additive genetic variance.

Suppose we have two islands, side by side. On both of the islands, some people are taller than others.
It so happens that we know (God told us) that there is a particular gene which can make a difference to your height: all else being equal, As are a foot taller than as. It also so happens that we know (God told us) that coffee stunts your growth; all else being equal, people who drink tea are a foot taller than people who drink coffee.
(We also happen to know that, at this moment, there aren't any other factors contributing to variation in height. Convenient!)
Now to our islands.
On the Blue island, we see that some people are taller than others. We do some testing, and we find out that on this island some people are A and others are a. In contrast, we also find that everybody on this island drinks tea and nobody drinks coffee.
There is variation in height: all of it is due to variation in genes, and none of it is due to variation in choice of beverage. Heritability = 1.
But that doesn't mean that the environment isn't relevant to height in this case. On the contrary, we happen to know (God told us) that if they'd all drunk coffee instead, they'd all be a foot shorter.
On the Red island, we see that some people are taller than others. We do some testing and find out that all of them are a's; none of them are As. In contrast, some of them drink coffee and some of them drink tea.
There is variation in height: none of it is due to variation in genes, and all of it is due to variation in choice of beverage. Heritability = 0.
But that doesn't mean that genetics is irrelevant to height in this case. On the contrary, we know (God told us) that if they'd all been As instead, then they'd all be a foot taller.

The most convincing way to remind yourself why heritability isn't about "how genetic a trait is", I find, is to remember that if everyone has the gene, then the gene doesn't vary, and won't contribute to variation; but that doesn't mean the gene isn't relevant!
For example, as far as I know, there is no genetic variation for "having a heart". Everyone is born with a heart. People without hearts are missing hearts because of environmental factors such as this:

So having a heart has a low heritability, but that doesn't mean genes aren't involved in building hearts!
Likewise, a high heritability doesn't mean that environmental effects aren't important to the trait; it just means that differences in the environment aren't currently contributing to differences in the trait.
It also doesn't mean that future environmental factors might not become important. For example, the heritability of eyesight was presumably somewhat high. But that didn't stop whoever did it from inventing glasses!
So that's another lesson. Heritability is not a constant. Natural selection actually tends to push heritabilities down (since it gets rid of the worse genes); and if the environment changes, then the heritability can go up down or all over the place.

Briefly, because remi.b gives a lot of good detail about this in his answer, (narrow sense) heritability is essentially a measure of how much of the phenotypic variance is explained by (additive) genetic variance. Phenotype (P) in an individual is the result of genetic (G) and environmental effects (E).
$P = G + E$
Thus the within-population variance in phenotype is
$V_P = V_G + V_E$
Genetic variance further decomposes in to additive (A), dominance (D), and interaction/epistatic variance (I).
$V_G = V_A + V_D + V_I$
Narrow sense heritability ($h^2$) is then
$h^2 = \frac{V_A}{V_P}$
Additive genetic variance and, as a result, the narrow sense heritability can be zero for two reasons.
Firstly, if no genes have an effect on your trait, then additive genetic variance will be zero.
Secondly, if the alleles at the loci affecting the trait are fixed within the population, additive genetic variance will be zero.
Therefore, Eric Turkheimer is correct to say that heritability is not a measure of how genetic something is. However, a heritability of zero does not mean that something is not genetically controlled, just that there is no variance in the effects of genes.
To follow from the example of having two arms, clearly having arms is genetically controlled, its a heritable trait, but the number of arms has very little/no genetic variance. Very few people have >2 or <2 arms, thus any allele for that seems to be exceptionally rare (the alleles determining that two arms are produced are more or less fixed, $p \approx 1$, where p is the frequency of the allele coding for two arms).
The following graph shows the effect of allele frequency on additive genetic variance, additive genetic variance is zero when the locus has a fixed allele, and maximised when the frequency of both alleles (a two allele model) 0.5. In practical terms, when p = 0.5, half of the population are heterozygotes, one quarter are homozygotes for allele 1, and one quarter are homozygotes for allele 2.

For example, in this study, we showed that genetic variance on the Y chromosome explained only ~0.4% of the variation in lifespan, which could be because very few of the genes affecting lifespan are on the Y (likely, because the Y contains very few genes, while lifespan is highly polygenic) and/or the genes on the Y affecting lifespan have low polymorphism (likely, because the Y is subject to various processes that greatly reduce within population molecular variation, compared to other chromosomes).
Heritability and additive genetic variance are important to understand because they determine the rate at which adaptation (evolution as a response to selection) can occur. Following Fisher's fundamental theorem, and as shown in the breeders equation ($r = h^2s$ where r is the response and s is selection), when $V_A = 0$ the $r = 0$.

Very good reviews of the overall concept have been posted, but I would like to focus in on the soft question of in what ways heritability does not reflect "how genetic" something is.  Of course, that's not really a technically defined statement and in some ways it does, but let's stick to the question:

Environmental contributions vary.  Consider pulmonary fibrosis.  A certain low rate of familial pulmonary fibrosis will always be present due to genetics.  But in a town built around a coal mine, you expect to see a much higher level of idiopathic pulmonary fibrosis.  You could argue the semantics, but probably traits related to this condition are not "more genetic" in the towns without coal mines.
Genetic contributions depend on environment.  The correlation of cognitive deficits with phenylketonuria alleles is quite high under some conditions, but with appropriate diet and supplements these genes have much less influence - "reduced penetrance", you might say.  Is PKU "less genetic" depending on nutrition?  Perhaps eye-tracking software will lead to a new sort of gaming next year, and as "eyethletes" suffer misfortunes the heritability of some ophthalmic traits will plummet, but does that mean the genes are weaker?
Not all genetic contributions are known.  Before the HIV pandemic, delta32 CCR5 would not have been recognized to have an effect on immunosuppression (at least, not by that means).  So we may not truly understand the genetic component that potentially exists even after thorough study of the trait under present conditions.

authors: user1205901 - Слава Україні


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Are there medical treatments that were so effective they were never subjected to a randomized control trial?
I'm thinking of things like antibiotics for meningitis or tuberculosis, or thiamine for Wernicke-Korsakoff syndrome. In those cases the magnitude of the treatment effect might have been so great that it would have been unethical to assign subjects to a placebo group. However, I couldn't find any sources to attest that randomized control trials were never done in relation to those treatments.
I'm referring to treatments trialled in a time and place in which randomized control trials were an option.

there were no clinical trials in olden days

In Japan, the government approved some chinese medicine without clinical trials, even if the system to approve drugs has been already established for a decade by referring to the system by western countries. The medicine is still covered by insurance.

Most surgical medical treatments fall into this category.  For example, patients with acute appendicitis who do not receive an appendectomy will die from peritonitis.  Also, it is difficult to obtain ethics approval for an RCT where you open up a person and then sew them back up  simply as a sham treatment.

Often new treatments are compared against best available treatment rather than placebo to alleviate ethical issues.

In recent years, clinical trials are all necessary. You have to have the randomised control To make sure it isn't a placebo effect. If and only if the drug seems to be super effective will they cut the randomised control short and give the real drug to everyone.
Sadly, while it may seem unethical, there was a cancer treatment that two cousins got into. The normal treatment guaranteed death, while the new drug actually had people practically bouncing off their death beds. One got the placebo - in this case normal treatment since it's unethical to not at least give standard care - and the other got the drug. The drug worked so well, the doctors tried to push to cut the trial short but they wouldn't and the one on the normal treatment died.
This drug was PLX4032.
blogspot uproar
clinical trial information
NYTimes article
So to my knowledge about clinical trials, no trial has been able to skip that stage. It's actually Called Phase III testing of the drug, followed by Phase IV which is administration to the public. It can, however, be shortened if it is promising enough.


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What color was the most recent common ancestor of all swans?
Was the most recent common ancestor of all swans black, or white, or some other color? How do we know, and how certain can we be?

Reptiles are thought to be the common ancestors of birds. Their skin color is not known, as that does not appear in the fossil record.

Your comment made me realise I'd phrased the question imprecisely. I've edited it to put in the words "most recent".

According to the known phylogeny of Anserinae in this paper,

Cygnus atratus (the black swan) is most closely related to Cygnus melanocoryphus (the black-necked swan). All of the other swans in the genus Cygnus are white, or close to white.
Therefore, it is reasonable to assume via maximum parsimony and maximum likelihood that the two genera evolved their blackness from a white ancestor, and not that all of the swans independently turned white from a black ancestor.

authors: user1205901 - Слава Україні


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When birds fly in V-formation, how is it decided which bird gets to be the 'lead bird'?
I've read on Wikipedia and in other sources that the lead position alternates due to flight fatigue, but does it alternate between a small cabal of of leadership birds, or does (almost) every bird get to sometimes go first?
Is the process different across different species?

There is an advantage for birds to fly in a V-Formation as stated by Portugal et al, 2013:

As a bird flaps, a rotating vortex of air rolls off each of its
  wingtips. These vortices mean that the air immediately behind the bird
  gets constantly pushed downwards (downwash), and the air behind it and
  off to the sides gets pushed upwards (upwash). If another bird flies
  in either of these upwash zones, it gets free lift. It can save energy
  by mooching off the air flow created by its flock-mate.

There is no advantage to the lead bird though, only the birds behind will get these free lifts by being in the upwash zones.
A study on Ibises determined that there was no clear lead bird and birds cycled between positions. Flying in a V-formation is a collective effort, there would be no benefit to always being in front, so the birds take turns. I would assume the same aerodynamics and the cycling of lead bird apply to all birds that generally fly in V-formations such as Geese. Otherwise the lead bird would just exhaust itself and not have enough energy to complete the migration, it would be the same situation as if the bird was flying alone.

By carefully observing the flock, the investigators learned that the
  amount of time a bird is leading a formation is strongly correlated
  with the time it can itself profit from flying behind another bird.
By working together, a flock of birds is greater than the sum of its
  parts. By not being selfish, individual birds can reap the collective
  advantage of aerodynamic wash-up, while also allowing for larger
  flocks, which result in yet more time for an individual to be in a
  backdraft situation.

Additional Reading:
http://phenomena.nationalgeographic.com/2014/01/15/birds-that-fly-in-a-v-formation-use-an-amazing-trick/
https://io9.gizmodo.com/why-birds-take-turns-at-the-front-when-flying-in-v-form-1683465294
References:
Portugal, Hubel, Fritz, Heese, Trobe, Voelk, Hailes, Wilson & Usherwood. 2013. Upwash exploitation and downwash avoidance by flap phasing in ibis formation flight. Nature http://dx.doi.org/10.1038/nature12939


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Prevent biofilm formation on moist surfaces
I have an indoor fountain with lots of water. What are the most common microorganisms in this kind of moist environment, and what are the standard way to prevent biofilm formation by them? I thought of copper and/or salt as general cheap disinfectants so far.

Bleaching powder can also be used but it can corrode metal parts. Salt will also aid in corrosion. You can try little bit of phenol or other aromatic disinfectants.

By salt about 3-4000 ppm is recommended. It starts to corrode most of the materials above 5-6000 ppm (from non scientific source). I read that cleaning it with acetic acid and using distilled water could work either. Algae is an usual microorganism in this kind of environment.

Distilled water is costly.. It will accumulate minerals and dust soon. You can occasionally use bleaching powder to clean it up. Better than acetic acid. Chlorination is commonly used technique against algae (bleaching powder is calcium hypochlorite).

Don't pools use chlorine tablets?

@Superbest This is an indoor fountain, and chlorine have an odor, so I wouldn't use it if not necessary. I stay with the salt (about 10-15 g/L), and see what happens. The fountain is 2 days old and does not get too much light, so I hope it won't bloom for a long while.

You can use some antibiotics or germicide or alcohol...they prevent the formation by interfering with the attachment or adhesion and expansion of immature biofilms..

Antibiotics degrade quickly. You would spend a lot of money on them if you regularly treat the whole water reservoir. Alcohol needs to be at a very high concentration (70%) to have bactericidal effect.

Antibiotics are expensive, and I don't want to nurse AB resistant strains. Germicide is a broad term... Alcohol is expensive as well, and will vaporize very fast. At least I get drunk ;-)

@inf3rno you could also use ion coatings...

How can I do that?

@inf3rno I think it comes as a spray... It's about $30...

Never heard of it...

@inf3rno http://www.righttoolusa.com/p/Sonus-Ion-Paint-Coating-55330570.html?gclid=Cj0KEQiAwaqkBRDHx6rzxMqAobgBEiQAxJazJ3jzHjOpHllIxRodywVckR6v5iXnefsLg0IlCPNgfYoaAofh8P8HAQ

@inf3rno it's kind of expensive...

@TAbraham Not exactly what I wanted, but would be good surprise to my father for xmas.


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What is the role of RAGEs?
According to articles I read, AGEs (advanced glycation end products) activate RAGEs (receptors for AGEs). This activation increases the ROS (reactive oxygen species) levels in the cells.

2003 - Reactive Oxygen Species-Regulated Signaling Pathways in Diabetic Nephropathy

Free radicals can cause damage in cells, which is definitely not good. What do you think, what is the role of RAGEs, which is more important than cellular damage?


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Does creatine-phosphate (CP) supplementation regenerate NADH?
I have the following facts:

It is possible to convert ATP <-> creatine vice-versa. (ref - non scientific)
CP supplementation protects against metabolic syndrome. ref1 ref2
Fructose digestion depletes NADH via TG synthesis. ref

I assume that CP supplementation regenerates not just ATP, but NADH, if it is depleted, and so it restores the redox balance in the liver. Both ATP and NADH are similar energy storing molecules, so I guess there is a biochemical pathway which converts ATP to NADH, or there is a pathway, which regenerates NADH using CP. Am I right, if so, which pathway is it?
note:
I might be wrong. From one of the references:

Taken together, this study provides direct evidence that creatine reduces lipid accumulation in hepatocytes by the stimulation of fatty acid oxidation and TG secretion.

So maybe ATP is enough to prevent TG accumulation in the liver.

Creatine itself is never converted into ATP. Creatine-phosphate on the other hand can donate its phosphate group to ADP, phosphorylating to form ATP and creatine. This is a buffer system for high-energy phosphates, and is very important in organs with rapid ATP turnover, notably muscle.
The mechanism of the findings described in the papers is not fully understood yet I think. But it is not via ATP, because the supplementation is not creatine-phosphate, but creatine itself, which does not yield ATP.
Regarding NADH: ATP is very different from NAD/NADH in terms of molecular structure, and the two are not interconverted by any pathway that I know of. (Probably this is not what you meant, but just to be clear.) But it is certainly true that reducing power in the form of NADH can be used to phosphorylate ADP into ATP; this is the task of the mitochondrial respiratory chain, where NADH is oxidized to NAD by complex I. On the other hand, I am not aware of a physiologically relevant process that uses ATP to reduce NAD into NADH.
The liver is a main site of synthesis of creatine itself, and this syntesis consumes methyl groups donated by the S-adenosylmethionine system. The authors of your ref1 seem to suggest that reduced synthesis of creatine following supplementation is a possible mechanism. Similar effects have been observed with choline supplementation, but again this effect is not well understood and a current research topic. A recent review is found here.

Creatine supplementation maybe increases the high energy phosphate reservoir. By "stimulation of fatty acid oxidation" I think they mean that the hepatocytes degrade fatty acids to produce energy for the conversion of creatine into creatine-phosphate. It would be interesting to check the regulation of CP synthesis, but I have no time for it currently.

I agree with @inf3rno that the creatine supplementation might increase the high-energy phosphate reservoir – this is the physiological basis for creatine supplementation in athletes. However, I know of no study whatsoever that has ever shown that we have been able to increase the reservoir of creatine phosphate by supplementing with creatine in the diet – this is the reason athletes take the supplement but there's no data (That I am aware of) actually suggest that it works the way we think it does


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Is there muscle hyperplasia or hypertrophy after surgery?
After exercise there is hypertrophy only. I am curious, if a surgery removes muscle, will there be hyperplasia or hypertrophy to restore it?

It does not required much research to find the answer. After injury and surgery the muscle undergoes inflammation to clear up the debris. After that myogenic cells start to proliferate and differentiate, so as expected, there is hyperplasia by restoring injured muscle. Which means that the body can fully restore muscle function if the injury is not too severe.

Effective fiber hypertrophy in satellite cell-depleted skeletal muscle.
Cellular and Molecular Regulation of Muscle Regeneration
Regeneration of mammalian skeletal muscle. Basic mechanisms and clinical implications.

I investigated this a little bit further. Muscle regrowth is mediated by the BM (basement membrane) which is the extracellular matrix that sorrounds the muscle fiber. If that is badly damaged or the nerve is cut, then the muscle fiber won't grow back and we will get scar tissue instead. The muscle will compensate this at a certain level by hypertrophy. There is an interesting new treatment for severe muscle injury, which removes the scar tissue and adds pig extracellular matrix to regrow the muscle.

Implant Lets Patients Regrow Lost Leg Muscle

"Which means that the body can fully restore muscle function if the injury is not too severe" – as far as I remember, connective tissue proliferates a lot faster and most of the damage is "hot-fixed" that way, that is musles do not fully regenerate their physical capacity, unless the damage is very localised and limited. I might be wrong though: I only had two basic courses on morphology and histology many years ago.

@EliKorvigo Well we can find it out.

@EliKorvigo I read yesterday that muscle can grow back if the basement membrane is not removed. I just need to read a little bit more in the topic.

@EliKorvigo As far as I remember healing has nothing to do with how fast a tissue type proliferates. It depends on what type of stem cells you have and what signal they get. But maybe I am wrong. I have only superficial knowlegde in the topic.


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Why are sarcomas rare compared to carcinomas?

A sarcoma (from the Greek σάρξ sarx meaning "flesh") is a cancer that
  arises from transformed cells of mesenchymal origin. Thus, malignant
  tumors made of cancellous bone, cartilage, fat, muscle, vascular, or
  hematopoietic tissues are, by definition, considered sarcomas. This is
  in contrast to a malignant tumor originating from epithelial cells,
  which are termed carcinoma. Human sarcomas are quite rare. Common
  malignancies, such as breast, colon, and lung cancer, are almost
  always carcinoma.

ref: https://en.wikipedia.org/wiki/Sarcoma

I was wondering why most of the tumors come from epithelial cells?

https://clinicaltrials.gov/ct2/show/NCT00029991 I have found something interesting. "These cells, known as endothelial cells, are susceptible to damage by blood cholesterol, smoking or high blood pressure and, when damaged, will allow cholesterol to deposit in arteries. Antioxidants can prevent the endothelial cell damage" - So antioxidants might prevent cancer by protecting endothelial cells from being damaged by carcinogens. If so, then atherosclerosis and high LDL cholesterol should be a risk factor of cancer. I don't remember reading of such a connection...

According to many articles and wikipedia as well obesity is linked to cancer. http://cancerpreventionresearch.aacrjournals.org/content/3/11/1451.short http://link.springer.com/article/10.1007/s11912-010-0139-7 http://www.sciencedirect.com/science/article/pii/S014067360860269X According to this article fat on its own is not the cause of the cancer but changed metabolic state might be. http://cancerres.aacrjournals.org/content/67/6/2391.short

So the previous articles indirectly support that endothelial damage causes cancer.
Another interesting topic is: https://en.wikipedia.org/wiki/Surface-area-to-volume_ratio The endothelial tissue has a high surface/volume ratio, so it might come in contact with potentially damaging compounds more often than other tissue, since these compounds tend to travel through blood. However I don't feel this a complete explanation. I think endothelial tissue is more prone to cancer somehow genetically. Probably cancers caused by ionizing radiation support this somehow, because they are not blood related.

Note that epithelial and endothelial cells are two different lineages. Carcinomas derive from epithelium. Tumors originating from endothelium are considered sarcomas, and they are rare. See https://en.wikipedia.org/wiki/Angiosarcoma


text:
Is it possible to transfer acquired hemophilia with breast milk?
There is a transplacental form of acquired hemophilia: http://www.jpeds.com/article/S0022-3476%2895%2970132-X/abstract
This disease is caused by polyclonal immunoglobulins (IgG1 and IgG4) against the A2 and C2 domains of factor 8. So acquired hemophilia is an autoimmune disease. By the transplacental form the maternal IgG antibodies causing this disease in the newborn. As far as I know IgG antibodies are transferred with breast milk too. Can breast milk cause this disease?

Acquired Hemophilia is an AutoImmune Disease, hence it is possible to transfer it from mother to child through breastfeeding milk. The antibodies subjected to autoimmune disease also passes into the infant or baby from breastmilk in addition to the healthy antibodies. These abnormal antibodies will act as an inhibitor to the enzyme responsible for production of Factor VIII , a blot clotting protein. Less number of factor VIII protein results in increased amount of internal bleeding.

Thanks James! The question was not about explaining what this disease is. Do you have any proof that it can be transferred to the child with breast milk?


text:
Is there any difference between microplastics from health perspective?
I wonder if there is difference between plastics if we talk about the negative health effects of microplastics. For example wood is just a bunch of polymer and some other components from chemical perspective and it is neutral from health perspective if it is not fungus infected. So I wonder if the polymer type matters by microplastics or it is just the size and maybe endocrine disruptor additives like BPA.

What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

@MattDMo Well I found some article that talks about different polymer types and has a hazard model, but it is for marine life. I did not find an article which assesses human health risks of different polymers. https://www.sciencedirect.com/science/article/pii/S030438942200187X I found another article for human health, but it is too general, no cell tests, etc. https://link.springer.com/article/10.1007/s40572-018-0206-z

it would be helpful to have those citations directly referenced in the question, noting your specific objections to each and why they don't answer the question.


text:
What is the numbering convention followed in the reverse strand of a DNA sequence?
The start and end location in forward strand is from 5' to 3' end. Can anyone confirm if the start and end location for genes on the opposite strand, as mentioned in the GTF gene annotation files, the start position is interpreted from the 3'->5' end  or 5'->3' end as illustrated below ?

Summary
There is a single numbering scheme for the base-pairs in the DNA sequences of  genomes. Numbering is from left to right in an agreed, but fundamentally arbitrary, standard orientation for a reference genome (or its chromosomes). Annotated genes assigned to a position within a genome or chromosome may differ in the direction of their transcription, but this is not indicated by any change in numbering, but by some other means. In the GFF/GTF file format a ‘+’/‘–’ system is used to indicate the ‘left-to-right’ (aka ‘forward’) or ‘right-to-left’ (aka ‘reverse’) directions of transcription, respectively.
Clarification of the question
The question refers to the 5′→3′ ends of a genome, whereas 5′→3′ is a direction. The term 5′- and 3′-ends can only be applied to a single strand of a nucleic acid, not to a double-stranded genome.  Furthermore a gene is not located on one or other strand of a genome. Because of these ambiguities, and my difficulty in following the diagram, I shall rephrase the question as:
“Does the numbering scheme for gene annotations within a chromosome differ depending on the orientation of the gene?”
This allows for a broader and more general answer, not restricted to the GTF format with which the poster is specifically concerned. However, I have tried to be precise and unequivocal in my terminology, and welcome comments from anyone who wishes to query or improve it.
Numbering and terminology for double-stranded linear genomes

Double-stranded linear genomes are numbered from one of their physical ends. For any genome there is an agreed reference orientation, although the choice of this orientation can be regarded as arbitrary in absolute terms. In the case of human chromosomes, numbering starts from end of the short arm of each chromosome.
The genome in the reference orientation is visualized horizontally, starting on the ‘left’ and ending on the ‘right’. If both DNA strands are represented (by lines or by letters) then the strand running 5′→3′ is generally visualized above that running 3′→5′ (as in the diagrams in the question).
Data files (and authors) use different terminology to refer to the two strands (see below), but I prefer — and shall generally use — the descriptive terms ‘forward’ and ‘reverse’ for the strands running ‘left-to-right’ (5′→3′) and ‘right-to-left’ (3′→5′), respectively, as they are independent of any functional annotations that may be imposed on parts of the genome.
Although this numbering would also apply to the strand that has its 5′ end on the ‘left’ if it were a single strand, in my opinion it is better to think of the numbering in terms of numbering of base pairs. Thus, genes with different orientations (to be defined below) are generally shown adjacent to a representation of the numbered nucleotide sequence, rather than associated with a particular strand.
Nevertheless, the nucleotide sequence of only one of the strands of a genome — the ‘forward’ strand — is maintained in databases such as GenBank.
Numbering starts at ‘1’ for the first base-pair. (Computer scientists writing software to manipulate sequences tend to dislike this as they generally number strings from’0’.)

These points are illustrated below in a screen-shot of the extreme left of human chromosome 5 in the NCBI genome browser.

Gene orientation
The phrase in the question, “genes on the opposite strand”, though ill-chosen in my opinion, is an obvious reference to the fact that we consider that the genes assigned to parts of the genome are considered to have orientation or directionality, and that there are two possibilities in this respect: running ‘left-to-right’ (in relation to the standard visualization of the parent genome) or in the opposite direction (right-to-left).
What is the basis for assigning such an orientation? Often (as in the phraseology of the question), this is related to interpretation of the potential for expression and the relationship of the conventional direction in which the products of expression are written to that of the two DNA strands of the genome. This runs into problems of different types of product (mRNA followed by protein, or stable RNAs) and that the direction in which these are conventionally written is essentially arbitrary. In fact, I think it far better to consider this in relation to the direction of transcription, a process that involves physical movement of an RNA polymerase in a specific direction from a promoter sequence. This can be illustrated in the figure below, modified from Alberts et al.. which embodies the essential point that transcription proceeds in a particular direction from a (asymmetric) promoter sequence (p).

It is worth emphasizing that only one of the two strands of DNA of a gene is transcribed into RNA by DNA-dependent RNA polymerase. This, is what I prefer to refer to as the ‘anti-sense’ strand of the gene (the term cannot be applied to the genome), and results in a transcript which is an RNA copy of the ‘sense’ strand,  i.e. the DNA strand that ‘reads’ from 5′→3′ in the same way as the mature RNA (except for the substitution of U for T). (If the RNA transcript is a mRNA, the amino acid sequence of the protein product also has the same directionality as the ‘sense’ strand.) This is illustrated in the diagram below.

Gene orientation and NCBI file format
The NCBI website distinguishes between genes in different orientations by appending ‘complement’ before the number co-ordinates if the direction of a gene is in the reverse direction with respect to the genome:

The designation, ‘complement’. is not frequently employed elsewhere, but refers to the fact that the direction is that of the complement of the forward strand of the genome, the sequence of which is that deposited in NCBI/GenBank. See also the sample GenBank record at NCBI.
Gene orientation and GTF file format
The GTF format is derived from the GFF format, which is a tab-separated machine-readable file format in which there is a column (field 7) to indicate the orientation. This may take values of ‘+’ for genes oriented in the same direction as the forward strand or ‘–’ for the those with the same orientation as the reverse strand.
NC_004354.4 RefSeq  gene    124370  126714  .   -   .   ID=gene-Dmel_CG17636;Dbxref=FLYBASE:FBgn0025837,GeneID:5740847;Name=CG17636;cyt_map=1A1-1A1;gbkey=Gene;gen_map=1-0 cM;gene=CG17636;gene_biotype=protein_coding;gene_synonym=Dmel\CG17636,EG:23E12.1;locus_tag=Dmel_CG17636
NC_004354.4 RefSeq  mRNA    124370  126714  .   -   .   ID=rna-NM_001103384.3;Parent=gene-Dmel_CG17636;Dbxref=FLYBASE:FBtr0112921,GeneID:5740847,GenBank:NM_001103384.3,FLYBASE:FBgn0025837;Name=NM_001103384.3;Note=CG17636-RA%3B Dmel\CG17636-RA;gbkey=mRNA;gene=CG17636;locus_tag=Dmel_CG17636;orig_protein_id=gnl|FlyBase|CG17636-PA|gb|ABW09315;orig_transcript_id=gnl|FlyBase|CG17636-RA;product=uncharacterized protein%2C transcript variant A;transcript_id=NM_001103384.3
NC_004354.4 RefSeq  exon    126626  126714  .   -   .   ID=exon-NM_001103384.3-1;Parent=rna-NM_001103384.3;Dbxref=FLYBASE:FBtr0112921,GeneID:5740847,GenBank:NM_001103384.3,FLYBASE:FBgn0025837;Note=CG17636-RA%3B Dmel\CG17636-RA;gbkey=mRNA;gene=CG17636;locus_tag=Dmel_CG17636;orig_protein_id=gnl|FlyBase|CG17636-PA|gb|ABW09315;orig_transcript_id=gnl|FlyBase|CG17636-RA;product=uncharacterized protein%2C transcript variant A;transcript_id=NM_001103384.3

(Values of ‘.’ and ‘?’ are also possible.)
Although convenient for data files, I discourage the use of ‘+’ and ‘-’ as descriptive terms because of their use in relation to the strands of single-stranded RNA viruses.
Footnote: Terminology for the DNA strands of genes
In an answer to a previous question on SE Biology I discussed the terminology of the two strands of the DNA of an individual gene, which I think should be considered in isolation from (and in ignorance of) the reference directionality of the genome on or in which it resides. The terminologies for gene and genome are clearly distinct.

GTF format is the same as GFF v2. The start and end fields are relative to the first position in the reference sequence which is assigned coordinate 1. The reference sequence, by definition, is the +/forward strand, so all coordinates are relative to the forward strand. The start coordinate will always be less than the end coordinate. If a feature is stranded (like a gene) the strand for the feature will be indicated by a '+' or '-' in the 7th field. Scenario A in your diagram is correct.


text:
Can the environment affect genes and adaptation in offspring?
I recently read several articles that believe that environment can affect gene expression and this change will transfer down to the children. Some theorists believe that random mutations are more rare and time consuming than a mutation that develops as a response to change of the environment the organism is in.
Epigenetics could be the key to how animals adapted and evolved so fast.
So does this mean a couple living in say, Siberia (both of whom migrated from say, Congo) will have higher probability of transferring gene variations to their children or grand children that will allow them to adapt better to the cold (as compared to the offsprings randomly developing mutations that help them adapt to the cold, and then passing it on to future generations)
Does that explain how humans were able to evolve quickly to their travels from Africa to the rest of the world and still survived the drastic changes in environment, rather than conclude that random gene variations led to adaptation?
Is this genetic adaptation as a response to the environment  biologically proven?
http://dukemagazine.duke.edu/article/big-question-can-your-environment-change-your-dna

Welcome to Biology.SE. I am afraid your question is very unclear. I have not read the linked popular article but I suppose you are talking about epigenetics. If yes, you should make this clear. random mutations are more rare and time consuming ... than what? gene expressions could be the key to how animals adapted this is very unclear. Does it mean mutations to regulatory sequences or are you still talking about epigenetics? higher probability of transferring gene variations to their children higher than what? I am VTC as unclear.

@Remi.b , edited the question with clarifications.

Offspring has no plural. (Oh, and the answer to your question is NO, but until you provide evidence to refute, this cannot constitute a SE answer.)

Generalities
You have misread the articles (or read misleading articles).
Epigenetic modifications are, by definition, any modification to the DNA and proteins attach to DNA that does not affect the nucleotidic sequence (note that I here ignore some of the difficulties defining the term epigenetics). Such modification include methylation of histon tails for example (a histon is a protein around which the DNA is wrapped). Those epigenetic modification can appears in reaction to the environment and can be passed on to the offspring giving it a seemingly Lamarckian style of inheritence.
A mutation is, by definition, a change in the sequence of nucleotides. An epigenetic modification is therefore not a mutation (and a mutation is not an epigenetic change).
Comments in the text

Some theorists believe that random mutations are more rare and time consuming than a mutation that develops as a response to change of the environment the organism is in.

You might want to avoid calling "mutations" "random mutations" because it feels like you might not understand how unclear this phrasing is. Have a look at the post Are mutations random?
Epigenetics change are NOT mutations.
The claim is too general and unclear and is impossible to comment about it without knowing what process you are interested in. One might claim that most genetic variance in populations is caused by epigenetic variation or make other claim that can be discussed but the above claim is too broad and unclear.

So does this mean a couple living in say, Siberia (both of whom migrated from say, Congo) will have higher probability of transferring gene variations to their children or grand children that will allow them to adapt better to the cold.

I don't understand what you mean here. And it feels to me that explaining everything that is unclear and going through all possible ways of understanding this sentence would take too much time!

Does that explain how humans were able to evolve quickly to their travels from Africa to the rest of the world and still survived the drastic changes in environment, rather than conclude that random gene variations led to adaptation?

You are really not using the term random correctly, which makes your question hard to understanding. Also, instead of gene variation I suppose you might want to use the term allele.
It is possible that epigenetics has played a role to allowing faster range expansion / range shift of human populations. I don't know if this is the case and I don't how important of an effect it would have.

Is this genetic adaptation as a response to the environment biologically proven?

Epigenetic, not genetic. Yes, epigenetic modifications do exist. We have plenty of evidences. I don't know how much we know about their impact on population range shift and survival but I would notice that it depends upon what mechanism exactly we want to consider into the broad term of epigenetics. For example, everybody will consider histon modification as part of epigenetic modifications. However, not everybody will want to consider fat content in the egg as an epigenetic modification. There is also a blurry border between what would be environmental effect (such as maternal effect) and epigenetic effect. But this is a discussion for another time.

Epigenetic modifications may exist in bacteria and in the differentiation of cells, but I have yet to see a study that shows environmental conditions can cause e.g. histone modifications in humans, and that these can be inherited. This seems to me to be the sleight of hand in all these popular articles. So no, this is not biological proven.


text:
Molecular/cellular biology textbook to consolidate what I know about molecular/cell biology
I'm a medical student (who is halfway through med school) looking for a textbook that will consolidate some of the biology I already know. While I've read a lot of books that go into great detail about genetics, immunology and cell signaling, I've not found many books that focus on clear insights.
After recently having perused a very well-written nanotechnology book geared towards bionanotechnology ("Bionanotechnology: lessons from nature," by Goodsell), I found many cell biology topics very well explained. For example, it states simply that "lipids are used for infrastructure [in the body]", and that "polysaccharides are used in specialized structural roles". Such sentences I've personally never really come across in any of the "standard" molecular biology texts (Alberts, Cooper, etc); I found that they focus far too much on detailing exactly the components of the DNA polymerase, or the ribosome (which are very important, but also something I'd like to go "beyond".)
Clarification on what type of book I seek:

A book within cell or molecular biology
Scope of book; a book that covers any of the following: biochemistry, genetics (replication, translation, transcription, gene expression and its regulation, epigenetics, heredity, genetic engineering), developmental biology, cell biology (cell structure, organelles, cellular processes, cell signaling) and molecular biology (techniques such as high-throughput biology; concepts such as enhancers, repressors) and molecular evolution.
Level of the book doesn't matter, although I have completed all the subjects above at an undergraduate (bachelor) level - the book could thus be directed towards graduate/masters students.

Any books/texts that will hone one's knowledge on the subjects mentioned will be warmly received!

my opinion... but, if you're half finished with medical school I'd work on understanding clinical medicine - there is plenty to work on there and you can always come back to intensive molecular biology/etc after you've mastered clinical medicine

While I find this has little relevance to my original question, I'm currently looking to do systems biology research alongside medical school. I feel that a stronger intuition for cellular processes will probably do some good for an aspiring clinician-scientist.

Please have a look the tag-wiki for [tag:book-recommendation]. If you do not address all the points mentioned there then your question may be put on hold. These kinds of questions often lead to opinon-based answers.

Campbell's Biology is, I quote my biology teacher, "the Bible of AP Biology". I know you're a medical student and therefore far past that introductory college level, but Campbell's does quite a good and thorough job of explaining a plethora of biology topics. It's a fairly reliable textbook, I think you might like it. It also gives a good deal of examples for the various concepts and avoids such abstract statements as those you quoted from your textbook. I would suggest skimming through the book at a local bookstore if you can and seeing if it fits your criteria.


text:
Hardy-Weinberg equilibrium generalized to add inbreeding (non-random mating)
Background
Quoting from Gillespie's book

The level of inbreeding is measured by the inbreeding coefficient, $F_I$, which is the probability that two alleles in an individual are identity by descent.

The two possible alleles are $A_1$ and $A_2$ and their frequencies are $p$ and $q=1-p$, respectively. Gillespie goes on and give the expected genotype frequencies given $p$ (and $q$) and $F_I$
$$
\begin{array}{r|c|c|c}
Genotype & A_1A_1 & A_1A_2 & A_2A_2 \\
\hline
Frequency & p^2(1-F_I)+pF_I & 2pq(1-F_I) & q^2(1-F_I)+qF_I \\
\end{array}
$$
Question
Can you please help me to understand why those are the appropriate genotype frequencies?
Example of what is unclear to me
By the definition of $F_I$, I was expecting that the frequency of `$A_1A_2$ (and $A_2A_1$) would be $(1-F_I)$, that is the frequency (or probability) that two alleles in an individual are not identical by descent. I feel like the definition given above is wrong. Should it rather be something like the weight for sampling like individuals? That is if there were only two possible mates, one that is $A_1A_1$ and one that is either $A_1A_2$ or $A_2A_2$, then the probability for a $A_1A_1$ individual to mate with the other $A_1A_1$ is $F_I$.

You're confused because you're failing to distinguish between 'identical' and 'identical by descent'. Some pairs of alleles would still be identical even in the absence of inbreeding.
We model the inbreeding by classifying allele pairs as IDB - always homozygous - or not IDB -  distributed according to Hardy Weinberg. The frequency of a pair of alleles being A1,A2 (or A2,A1) is thus the frequency under H.W.E. (2pq) multiplied by the chance of them NOT being IBD (1-FI). And conversely, a pair can be homozygous and not IBD - at frequency p 2(1-FI), or because they are IBD - at frequency p F I.

+1 Oh..ok! This is a little disturbing to me. The concept of IBD depends on an arbitrary time in the past beyond which if coalescence occurs, then we still call the two alleles IBS (Identical by state) and not IBD (I could cite Hartl and Clark I think but don't have the book with me today). Am I right?

Yes, but these models are just simple approximations. Concepts like time and coalescence don't even exist the perfect binomial world of Hardy Weinberg  :)

Ok. I don't feel 100% clear with the definitions of IBD and IBS so I just opened "Identity By Descent vs Identity By State". Thanks for your help


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

[0.36 0.48 0.16]

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

[0.4091 0.4091 0.1818].

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

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

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


text:
Surrogacy Post Fertilization
The wikipedia page on surrogacy highlights two main forms of surrogacy: Traditional Surrogacy and Gestational Surrogacy. Traditional surrogacy inseminates the surrogate mother with sperm, while gestational surrogacy uses in vitro fertilization to form an embryo from egg and sperm, which is then transferred into the surrogate mother.
It does not discuss whether surrogacy is possible after a natural fertilization has already taken place, such as if a woman becomes pregnant and then wishes, for whatever reason, to have a surrogate take the baby to term. Is this biologically possible? If it is possible, what is the mechanism? Also, if possible, is heightened risk a major reason it is not more common?

No, it is not possible. The problem is the fertilization which takes place near the ovary. It takes the new forming blastocyst about 4-5 days to wander through the fallopian tube to reach the uterus and 8-9 days in total to implant itself into the uterine wall. See the picture below (from the Wikipedia article on fertilization):

You would have to get the blastocyst out of the right fallopian tube, make sure it survives the procedure and then implant it into the uterus of a woman which is about in the same phase of their period (otherwise the uterus is not ready to allow implantation).
It is already hard enough to do in vitro fertilization where you can control the environment.

in other words...have you ever tried to find a fertile zygote in a fallopian tube?  the physician would have to be in there with a light and a microscope and some forceps...and its 0.1 mm in diameter! yow that sounds impossible and painful and interminable!

Thanks for the short version :-) And you would have to choose the right tube as well...

There are different types of surrogacy, but as you said the most common one are traditional and gestational surrogacy.
Traditional surrogacy normally involves intrauterine insemination (IUI), so the eggs of the surrogate are used in the surrogacy process. Once the fertilization takes places it's not possible to extract the embryo.
On the other hand, in gestational surrogacy the creation of the embryos is done via an IVF process, and once they are created they are transferred to the surrogate. So in this process, the fertilization process take place out of the surrogate body.
So, in summary, while gestational surrogacy uses a IVF technique to create an embryo that afterwards is transferred to the surrogate, traditional surrogacy uses IUI to artificially inseminate the gestational carrier. IUI is less complicated than IVF, and this process can be repeated several times until a pregnancy is achieved. However, it's not possible to make the fertilization in one woman and afterwards transfer the embryos to the surrogate, that would be extremely complicated.
Here you can get more info about the different forms of surrogacy.

Hi, welcome to the site!  I'm honestly not sure what this adds to what has already been said... and in a lot of ways this looks more like a comment than an answer.  Sure, it does very briefly answer the question (1 sentence with no backup other than "that would be extremely complicated"), but the rest of the answer is totally incidental to the question posed.  In the future, please try to keep answers directed specifically toward the question posed.  Thanks!


text:
Any examples of life forms on Earth that could have survived on Mars or Moon?
Do we know of any living forms on Earth that could continue to live on Mars?

Under the current conditions and without an athmosphere? Hardly imaginable.

Yes, under current conditions and without an atmosphere.

Yes, research studies that were conducted have found that methanogens (microorganisms) are able to survive in conditions similar to Mars (reference). Another study conducted has also concluded that some lichen and cyanobacteria is also capable of survival.  Surprisingly, they were also found to be active (reference).
There is speculation now on whether organisms from earth have been accidentally transported to Mars on the Mars Curiosity Rover which would be funny or a cause of concern, depending on how you look at it (reference).

Interestingly, methanogenes are even more useful for terraforming Mars than plants, because they accelerate greenhouse effect.