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When does the first "random mutation" of DNA (have to) occur?
When reading about how evolution happens, "random mutations" are often spoken of.
As far as I understand, "random mutation" refers to the unsuccessful self-replication of DNA (the new version of which is then passed on correctly). But when does this change happen? During fertilization? Shortly before (in the sperm or egg itself) or shortly thereafter? And what is the last possible time for that to happen so that it gets passed onto every cell in the body and eventually brings forth a new physical trait?
I hope the questions make sense, I don't have a lot of background in biology.
Edit for completeness: When is the earliest possible moment for a mutation to take place? (A mutation that will ultimately make it to the offspring and eventually cause a new trait.) Is it in the ovaries/testicles or even before that?

I think you will do better not to put things like random mutations in scare quotes. It immediately puts you in a category hostile to science.

Random mutations happen everywhere in the body all the time. Most are harmless, some cause problems, some cause cancer. Some are beneficial. If a beneficial mutation occurs in the germ cell line, it will be passed on to the offspring. Depending on how beneficial it is, it can spread like wildfire (the mutation allowing lactase to continue to be expressed after infancy is a good example of this, as is sickle cell trait); if it is harmful, the carrier may die before birth, in infancy, etc. If it causes a later onset disease (e.g. early Parkinson's)1, the carrier has time to mate, reproduce and pass the disease on to their offspring. More and more diseases are being found to be genetic in nature now that genetic studies are so much easier to perform.
Again, for a mutation to be passed on, it must occur anywhere in the germ cell line of a parent, right up to the last stage before being released as an ova or a sperm cell, during fertilization, or during the very early stages of embryonic development in cells genetically programmed to become germ cells. If it occurs after fertilization, it will not affect that person, but its offspring. Depending on how early the mutation occurs, it may affect other parts of the reproductive system as well.
If a mutation happens in an embryo in a non-germ cell line, it may affect that person mildly, profoundly, not at all, or the embryo may die if it is a deleterious mutation in a critical organ system, say the heart.
But you need not put random mutations in scare quotes. I'm pretty sure you don't trust me, but they happen all the time, in every tissue, in you yourself as well as in everyone you know and everyone you don't know. And, by the grace of God, many of them can be repaired, and we don't ever have any ill effects from them. Alas, not all are repaired, and some lead to cancer.
Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1

Thank you for this great answer! I'd love to upvote, but it doesn't let me. The first three paragraphs make a perfect answer in terms of what information I was looking for. Though the rest, dunno where that came from—was it because of the quotation marks? Haha, they were partly in the sense of "seeing this term often but not sure if established scientific term hence quoting it" and partly "not sure if this is what I want to ask about". Eventually comparable to how some technically less versed person might put quotes around "tablet" or "smartphone". Powerful little fellas.

The question had nothing to do with faith. Why include it in your answer.

I agree with @Floris comment. I think you let yourself react too much to the quotes around the term "random mutation" :) Also, you say Science and faith are not mutually exclusive. This is a question of philosophy and not science and should not be present on this website (or only as a tiny note that is clearly label belonging to philosophy and only if obviously aligned with the interest of the OP). Finally, not to be too picky but in the middle of these discussion, the use of the expression grace of God sounds quite inappropriate.

@Remi.b - That is a bit pickly. Have you ever heard the expression, "There but for the Grace of God go I?" It doesn't have a necessarily religious connotation anymore.

@KarloGrba - Sorry for the assumption!

@Karlo Grba, Hi, I like answers like this which is to the point. I had this question in mind for a couple of days. When biologists say humans have about 65 mutations per generation, it should actually arise mostly during the fertilization through meiosis and before large scale celluar differentiation which is a very short term like a few days. After the gametes are formed, mutations should be repaired like other normal cases(mutations are minority already). Is this what biologiests think? (I mean, mutations effective for evolution takes only in couple of days..!!)

You need to understand that whenever a cell duplicate there is a DNA replication process, which means even when you are growing up there is DNA replication process, whatever or wherever you are there is DNA replication because cells in your body don't stop duplicating, which means every cell duplication hold a risk potential of causing a DNA mutation but that potential's probability is as low as one in a billion cell duplication and even if there is any mistake in the DNA-replication process the DNA-Polymerize-enzyme have repairing abilities which correct the mistakes, well sometimes even  DNA-Polymerize-enzyme don't repair these mistakes which cause a disorder in some gene's task, these disorders might be helpful and make the creature grow faster or reproduce faster, or it might be harmful and cause diseases or some kind of three hand human or any kind of disorder and that depends on which gene that has been affected by the mistake in the DNA-replication, that means if the gene was in charge of the cell's duplication process this might make the cell duplicate forever and cause cancer, on the other hand, most of the times the mutation doesn't happen normaly because DNA-Polymerize-enzyme failed to do it's job but it happens because of some chemicals or even being exposed a lot of time to the sun rays. Bear in mind that fertilization or anytime before or after it have anything to do with DNA mutation as far as I know, anyway I might be mistaken, I have answered you by the information I got in the school.

so most people already know cells undergo muation and it is repaired. Of course these most (99.999%) mutation has nothing to do with evolution because it's not in gamtes cell and not related to reproduction. THe mutation in the gametes only affect next generation and the mutations before large scale cell differentiation of the gametes only affects DNA pass-down to the next generation, which is during only several days or weeks? I think this is against our intutition with the mutation proability and "65 mutations per generation" measurement.


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What are the consequences of drinking water with food?
Does drinking water with a meal release lesser energy/glucose into the blood stream due to a diluted digestive mixture ?
For simplification : If a person eats 100 grams of cooked jasmine rice with no water in take, when digested in 90 minutes  releases, say, a 100 calories. Then, if  the person eats 100 grams of cooked jasmine rice and drinks 50 ml of water along with it (during/after) (basically, halving the power of the digestive juices) then will the energy released be 50 calories ?

Cooked rice or dry rice? Cooked rice absorbs water, so even if you didn't 'drink' any water, you still would have ingested it.

@XaNaX edited question

A moderate amount of water while eating will not dilute digestion
...according to Michael F. Picco, M.D. and the Mayo Clinic:

There's no concern that water will dilute the digestive juices or interfere with digestion. In fact, drinking water during or after a
meal actually aids digestion.
Water and other liquids help break down food so that your body can
absorb the nutrients. Water also softens stool, which helps prevent
constipation.

Water, after all, is the "universal solvent" which should help break food and organic materials down further.
Effect of Stomach Acid Dilution
This is a total myth, especially if you consider it from totally a chemical perspective.  Stomachs secrete about 400 to 700 mL of gastric acids per meal. Just to be conservative, let's say 500 mL.  Also, the average stomach has a pH of about 2.  Now let's look at the formula for pH and what the effects of adding water might be:
pH = log(1/(mols/volume))
2 = log(1/(mols/0.5L))

Now solve for mols, and we get mols = 0.005
Now let's assume our meal contains about a quarter of a liter of water in it.  We'll also assume that our food is completely pH neutral.  This is probably a little high on water concentration, but let's see its effect on our stomach's pH.
Since it has a neutral pH, the mols does not change, but our volume does (0.5L [previous contents] + 0.25L [from the food] = 0.75L).
pH = log(1/(0.005 mols/(0.5L + 0.25L)))

Now solve for pH and we get pH = 2.18.  No problem here, since normal digestion occurs between a pH of 1.5 to 3.5.
Finally, let's say we drink a lot of neutral pH water with our meal now.
pH = log(1/(0.005 mols/(0.75L + 4.25L)))
pH = 3

So we are still within a normal pH of digestion, even though we just drank over 4.25 liters (~1.12 gallons) of water with our fairly liquid meal of 0.25L!  We would need to drink about another 45 L of water to knock our gastic pH above 4.  But don't worry, we would die of water intoxication well before that ever happens.
Furthermore, our stomachs (and digestive tract) are incredibly good at adapting their secretions to the consistency of a meal.
Water and Speed of Digestion
Perhaps another way that water may change caloric intake is to increase the speed at which solid foods exit the stomach.
This is thought to reduce the meal’s contact time with stomach acid and digestive enzymes, resulting in poorer digestion.
As logical as this statement may sound, no scientific research supports it.
A study that analyzed the stomach’s emptying speed observed that, although liquids do pass through the digestive system more quickly than solids, they have no effect on the overall solids’ digestion speed.
Bottom Line
Water during meals should not decrease the amount of calories absorbed.  With all that being said, digestion is a very complex system, and there are still many unknowns as well as individual responses.  Before making drastic changes concerning your health and digestion, you should consult a medical professional.  This answer should in no means necessary replace any medical advice or treatments, but rather aid in your understanding of how digestion works.
A Final Word of Caution
I feel obligated to include that however you found this question/answer, staying hydrated to aid in digestion is a very healthy function, especially in considering weight loss and 'feeling full for longer.'  However, obsessive water consumption aimed at decreasing food consumption/appetite ("fluid loading" or "water loading") is a common symptom of eating disorders.  If this is a concern for you or someone you know, please, seek professional support and help.

Sources:

NCBI - Adaptive Secretions

NCBI - Digestion Speeds

www.mayoclinic.org

water.usgs.gov

Thanks for answering. I am more interested in know if somehow (say by drinking half a litre of water) I am able to dilute digestion - will the process of digestion release only half the energy (carbs/fats/etc) from the food ?

@happybuddha no, drinking water will not decrease the amount of energy released from food by digestion. Any excess water will simply be absorbed by your body. There are no magic tricks.

I would suggest removing/rewording the last few sentences of your "Bottom Line" section - that's bordering on medical advice, which is off-limits on this site. If you are going to keep it, please add some supporting citations to show that the majority of acid reflux cases improve with more stomach acid. You also need to support your statement that one should delay drinking water until after a meal - neither one sounds scientifically accurate.

Now edited.  I originally included that part as a way to indicate this answer should not be interpreted as medical advice and there is anecdotal evidence (albeit, no peer-reviewed articles from my cursory search) suggesting the contrary - that water during meals has impeded their digestion, such as perpetuating their acid reflux.  Apparently this inclusion did the opposite of my intention.  These edits now directly state that this answer is not medical advice.

@MattDMo I am not looking for magic tricks - just a definitive answer !

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When to decide that two similar sequences are different genes or not?
Working on RNA-Seq data directed me to ask this question. In RNA-Seq jobs, after de novo assembly we have lots of transcripts with different rates of similarity (0 to almost 100 percent) that we sometimes don't know their loci.
So regardless of locus, on what reasons we differentiate two or more sequences?
How can we differentiate alleles of a gene from paralogous genes?
I hope my question is clear enough.

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What determines if an allele is dominant or recessive?
Going back to my high school days we were taught about dominant and recessive genes. We were taught how to calculate the geneotype and pheneotype of potential offspring using a small table (forgotten the actual table name). But it never occurred to me then what determines if a gene is dominant or recessive and how this is carried out biologically.
Take my example below, there is a 50% change that an offspring will carry both the tall (T) and short (t) genes. What determines that the tall gene T has a dominant effect over the short gene t.
Now, I know that there is going to be differences between the different genes (i.e. eye colour), but is there a general description any one and provide which states how a gene becomes dominant and how the dominant effect is carried out biologically.

A common cause is haplosufficiency, i.e. that a single copy of an allele will produce enought protein to create a heterozygote phenotype that is similar to the homozygote phenotype.

Which "why" are you asking? Do you mean "Why" like "why did it evolve that there is dominance rather that additivity?" or "why" like "what genetic mechanisms creates a relation of dominance between two alleles?"

If "why" meant "what evolutionary reasons" then, there are maybe two models that are worth talking about which are Fisher's model and Wright's model of the evolution of dominance

An interesting example I like is that horns on cattle is recessive, but having horns gives enough of an advantage that the trait became very common. But if you have a bull with two copies of the dominant no horns allele, none of your calves will have horns. Just an example that recessive traits aren't always rarer in nature.

Dominance is seldom complete. Owing to effects like co-dominance, incomplete dominance, collaborative (additive) effects of polygenes, our classical concept of dominance doesn't work. Having said that, there are certain ways in which a gene, if showing complete dominance can be analysed from the molecular level.
In an individual heterozygous for a certain trait, the following possibilities exist:

Both the alleles, though different, code for a protein (which might be an enzyme or a regulatory protein) which is functional and is indistinguishable atleast in terms of its functions. In this case, no matter if the person is heterozygous or homozygous for either allele, the concerned protein will be in sufficient amounts and will always be functional. These alleles can be treated as the same allele while performing Mendelian analysis though their products might differ slightly, leading to formation of two (or more) functionally similar Alloenzymes (as opposed to Isozymes which are similar enzymes produced by genes at different loci).
Haplosufficiency. In this case, one of the two alleles codes for a functional protein and the other either codes for a non-functional protein (or does not code at all). But, even in heterozygous condition where only one allele producing functional protein is present, the amount of protein produced is sufficient to show the phenotype and hence, even in heterozygous individuals, enough protein is coded for by the single functional allele exhibiting the normal phenotype. If the two non-functional alleles are present as a homozygous pair, no functional protein is synthesised and hence the phenotype is not shown (i.e a different phenotype is shown). Here, the functional allele is Haplosufficient (able to produce enough protein in heterozygous condition) and is called the dominant since it expresses its phenotype both in heterozygous and homozygous conditions. this is pretty common.
Complete Haploinsufficiency. Here again one allele codes for a functional protein while the other does not. But this time, if the functional allele is present in heterozygous condition, then the amount of the protein produced is not at all sufficient and hence the phenotype is not exhibited. Here the non-functional allele is said to be dominant because heterozygous phenotype resembles the phenotype of homozygous non-functional allele (where no protein is synthesized) since the functional allele is completely haploinsufficient (unable to produce enough protein in heterozygous condition). This method is pretty rare.(e.g rare autosomal dominant dyskeratosis congenita)

If there is partial haplosufficiency /partial haploinsufficiency, the phenomenon of incomplete dominance can be explained. (heterozygous individual produces protein not sufficient for a full-blown phenotype but just a partial expression of the phenotype)
Here, "functional" refers to being actually "functional" as in case of flower colour (anthocyanin synthesis) or just performing certain kind of a conversion leading to a particular effect on thephenotype.

Fisher and Wright provided two different models in order to explain why newly arisen mutations tend to be recessive. I am not sure though if this answer your question!
Fisher's model

"...there is a tendency always at work in nature which modifies the
  response of the organism to each mutant gene in such a way that the
  wild type tends to become dominant."
  Given that most mutations are deleterious, there is selection to make fixed mutations dominant over almost any mutations that could appear.

Wright's model

"...mutations are most frequently in the direction of inactivation and
  that for physiological reasons inactivation should generally behave as
  recessive."

There are 2 physiological reasons.
1) Deleterious mutations are mutations that usually cause a protein to not work properly. Given that the kinetics of reaction is usually not linear but is a function which derivative is decreasing over the number of enzyme, if we divide by 2 the number of functionning protein, we divide by less than two the reaction rate. Therefore, a deleterious mutation is usually recessive.
2) The reagents of a given reaction are often the products of another one. If this other reaction is slow compare to the reaction that followed, diminishing the rate the following reaction will not have a big impact on the rate of the overall metabolic pathway. Therefore, most deleterious mutations are recessive.
More information here
Note that there is a correlation between the impact a mutation has on fitness and its recessivity (the worst is a mutation, the higher is its recessivity).


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What was the first piece of work in computational biology?
What was the first piece of work in computational biology? I'm ideally looking for a paper.
I am not interested in works that involve data management or data analysis but work that model biological processes through numerical simulations or numerical approximations of analytical results.

I can think of three types of work where computers are used. (1) Data management and analysis, (2) numerical simulations and (3) numerical approximations to analytical solutions. Are you interested in all 3 of them?

2 and 3. Less bioinformatics, more computer modelling and theoretical modelling. The scenarios where people didn't have a lot of data, just theories.

I edited this info in your post (+1). I suppose it might be a paper of neuroscience in the 1960s or some cellular automata kind of algorithm.

Growth model by Jacques Monod 1949. However, there are much older works in computational biology. Michaelis-Menten model was published in 1913. What is the point of your question? Are you asking when were numerical methods first applied to biological problems? In that case, you should look at some point after the development of computers. After 1945 perhaps.

for my money it's the Lotka–Volterra predator–prey model  first expounded in 1910, and extensively analyzed by 1925. https://en.wikipedia.org/wiki/Lotka%E2%80%93Volterra_equations

@RBarryYoung The simple Lotka-Volterra equations can be analyzed analytically (see this post), no need for numerical simulations.

Does phylogeny inference qualify ?

@bli, sure, why not, but I doubt you'll find any before 1950 ...

@Remi.b But "analyzed analytically" does not mean that it has a closed form analytical solution.  That might explain why I cannot seem to find an analytical solution anywhere online.  The post you linked to doesn't have it. Neither does the Wikipedia article. Neither do a bunch of academic articles I've checked (though their titles sound like they have it). Weird. But even having a closed analytical solution does not mean it is non-computational since the goal is to plot and evaluate it over time. Even for say Sin(t)*Cos(t-1) there's a lot of repetitive hand calculation, ie. computation.

Another nomination, if you include infectious disease epidemiology as part of biology and hence computational simulations of epidemics as part of computational biology:
Measles periodicity and Community Size, M. S. Bartlett, J. Roy. Stat Soc. A, 120(1), 1957.
The computations were run on the Manchester computer. Possibly the most entertaining part of the paper is the discussion afterwards from one of the computing assistants:

Mr. J. C. GOWER: I should like to describe in a little more detail the programme for the Manchester computer which has produced the results that Professor Bartlett has been discussing ... Owing to the fact that the computer makes not infrequent mistakes and in view of the apparent impossibility of getting an overall check ... it is necessary to repeat the calculations ... The random numbers are produced in batches of 64. Each batch is tested for divergence from the expected number of unit digits. If the test fails a new batch is produced and tested. If three successive batches fail the machine stops and hoots continuously.
Only once in the sixteen months during which the programme has been running have three successive batches failed ...

But the winner (also in population biology) might be the one linked in the comments to a Biostars discussion, Gene frequencies in a cline determined by selection and diffusion R.A. Fisher Biometrics 1950.  On p. 169 the author says

I owe this tabulation to Dr. M. V. Wilkes and Mr. D. J. Wheeler, operating the EDSAC electronic computer

(the tabulation is the solution of the differential equation $\frac{d^2 q}{dx^2} = 4 x (1-q)q$ with boundary conditions $q=1/2$ at $x=0$ and $q=0$ as $x \to \infty$); the Wikipedia page about EDSAC (linked above) claims

[Fisher's study] represents the first use of a computer for a problem in the field of biology

Welcome to BioSE and really nice to see such a prominent researcher as a contributor.

I don't believe you'll ever find the first work in bioinformatics (or computational biology, as you put it), however the field really began in the times of accumulating data about protein biochemistry. Computational biologists (before they had access to the computer) would be writing and analyzing morphologies and types of proteins with pencil and paper.
But you can go even further back than this. "Alignment" is another old technique used in bioinformatics. This is establishing the amount of similarity between two DNA sequences, or rather the degree of similarity between any two objects or data sets in computational biology.
Your question, though, asks for a scientific paper (one of the oldest) on bioinformatics. This is arguably  M. O. Dayhoff's paper: "A Computer Program to Aid Primary Protein Structure Determination." (1962)
This is the first formal paper that limits the scope of computational biology to the definition provided by this BioPlanet article and generally agreed by many:

Bioinformatics is the application of computer technology to the management of biological information.

Depending on your definition of computational biology (e.g. bioinformatics and mathematical modelling can be quite different), there is an oft-cited reference to Alan Turing's work after the second world war, modelling what he called "morphogens" in the emergence of mathematical patterns in nature. As I understand it he modelled diffusion of antagonistic and complementary hypothetical molecules in space and time. I'm fairly sure this is one of the first examples of using the very early computers, while they were still reminiscent of counting machines for biological problems.
I don't have an exact reference for you right now, but some google-fu of "Turing" and "morphogens" will drag something up.
EDIT: here's the paper, 1952 is the year to beat!:
http://www.dna.caltech.edu/courses/cs191/paperscs191/turing.pdf

Please note that - while Turing is famous, and he usually gets most credit - his (absolutely great) work was lacking multiple important pieces - and was not necessarily computational biology - and had very little influence on biological research. "Turing's morphogens" were discovered independently, with the inclusion of missing pieces, and shown computationally, by Alfred Gierer and Hans Meinhardt ( for historical perspective: http://dev.biologists.org/content/develop/early/2016/03/22/dev.137414.full.pdf )

yes, but in the paper Turing does say (p. 65) "The figures in table 1 were mainly obtained with the aid of the Manchester University  Computer."  But the precedence probably has to go to the Fisher 1950 population genetics paper discussed in the Biostars thread mentioned in the comments above, Gene frequencies in a cline determined by selection and diffusion/1/238.pdf

I don't have any idea about the first paper in computation biology (interpreted by me as papers that use computers and computer simulations to solve biological problems). However, some population ecologists were early in adopting computer simulations to solve population models. Your should look at Micheal Hassell, which I know was early in using computer simulations. One of his first papers is New inductive population model for insect parasites and its bearing on biological control. from 1969 (pdf), where models are simulated on the "Oxford KDF9 computer". His other papers and his collaborators could be a starting point.

There is some ambiguity in words; however "computational biology" is often used to stress that work extends beyond sequence information (and sequence derived properties) and data management (which would rather be described by "bioinformatics").
If the question is about the first work that used computer simulations, and algorithms to discover and mechanistically explain some complex biological problem, the work of Hans Meinhardt and colleagues comes very close to a first piece of computational biology.
For instance they discovered how patterns could form; Gierer et Meinhadt 1972, and other references contained in his obituary

Looks like an interesting author to consider. Could you give more info of the years of various publication and the type of work he did ("discovering the formation of patterns" is very vague).

Have you tried pubmed ?


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Identification of snake
Can someone identify this snake? Photographed in a home in Los Lunas, NM, USA.

Check out the Desert Kingsnake (Lampropeltis getula splendida).  It is native to New Mexico.

Source: Desert Kingsnake (wikipedia)

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Why were vegetation coverages not assumed to be affected by precipitation, humidity or temperature?
I am trying to understand the graph topology of the structural equation model (SEM) given in Figure 1 of Bisset et al 2023. It is stated in the paper that it reflects an a priori causal structure.

I am trying to understand why the SEM assumes that climate variables do not affect the vegetation coverage variables. It seems like basic plant biology that they are affected by precipitation, humidity and temperature. Did I miss something about the nature of the coverage estimates?
Why would vegetation coverage not be assumed to be caused (in part at least) by climate these climate variables?

EC: electric conductivity
OC: organic carbon

Probably mostly because people misuse these sorts of models all the time.

The title of the article is (my emphasis):

Linking niche size and phylogenetic signals to predict future soil microbial relative abundances.

To look at bacterial abundance, they generated models that look at factors that affect bacterial abundance. In this case, this is a mathematical model that is used to describe the effect (emphasis mine):

Whereas a number of multivariate methods are largely descriptive and more appropriate for exploratory analyses, SEM is able to test a network of causal hypotheses and is recommended for evaluation of multivariate hypotheses (Grace, 2006; Grace et al., 2012). Specifically, we used SEM because it allows the evaluation of simultaneous influences...
...The method is thus appropriate for establishing probable causality at the system (for example, climate-vegetation-soil-bacteria), rather than the individual level (for example, climate–bacteria).

So, they are generating a model that looks specifically at establishing a causal model for bacterial abundance only. This model does not seek to establish causality for other factors, such as vegetation cover, even though this might be related to some of the factors being investigated. In fact the models explain mathematically only the significant factors for bacterial abundance, and factors that are left out of the model have no effect in the system being described - basically Occam's razor being applied.
You could indeed examine vegetation cover using a variables used in this system, but you would need to establish a whole new mathematical model to do so, and you might well find that the variables are different or need other factors not shown in this model.

I disagree with you and the authors on how to proceed with causal inference (see Pearl 2009 for an introduction), but your answer clarifies why the authors might have thought to exclude this relation between climate and vegetation.

@Galen I agree, it doesn't make sense to a me either, but this is how the mathematical models work, for better or worse. The factors that they show in the model are explicitly the ones that affect the thing being looked at and explicitly exclude those that don't, even though from a logical sense it might make sense to include them. Basically aiming for a minimal component model.

I have substantial disagreements with you, but I don't think it will be productive to clarify and argue here. It just isn't a great venue for it. There is a rigorous approach to thinking about statistical models in conjunction with causality. The book I cited is a detailed account, but if you don't have the time/money for it you might find Science Before Statistics: Causal Inference to be a feasible investment at least to get the general idea.

@Galen I'm not a modeler or anything of the sort, but thanks for the link. I agree this isn't the right place for discussion of your point. I've had similar arguments with modelers in the past, with me in your position, so I totally understand where you are coming from.

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Did my wildlife camera take a picture of a lynx?
A wildlife camera took a photograph of an animal. Unfortunately this is the only picture my camera collected. This picture was taken in the central interior of British Columbia, Canada. The distance from the camera to the subject is a few meters, and the height of the camera off the ground was probably about 40 - 50 cm.

Is this animal a lynx? It looks like it might have those fine tufts on its ears and a reduced tail.

While I generally try to avoid cross-posting, I have started pooling my observations into iNaturalist. This photo can be found as Observation 110929888.

Any chance of examining the area for tracks?

No, unfortunately the snow was quite icy and compacted; found no tracks.

How about markings on the tree trunk? IIRC lynx will sometimes scratch the bark as part of marking their territory ...

I didn't notice, but I wasn't looking for that. Interesting ethology fact though. I'll take a look at the trees in the area when I return to the location.

I thought that those cameras take a photo every second when something starts moving. It's facing towards the light as well so with the snow, it's too bright. The silhouette is definitely that of a lynx though, small tail, strong hind quarters, it looks like 90% probability it's a lynx

I have not played with the settings on this camera, but I recall from the manual that I can control the rate. I don't recall what it is currently set to, but I have a feeling it isn't as a frequent as every second; something I should correct.

As with your other trail camera question about coyote, some (fairly accurate) size estimate of the tree or other foliage in the picture may help. Lynx are typically larger than bobcats.

It is either a Canada lynx or a bobcat.
From wikipedia:

The lynx is between 73 and 107 cm (29 and 42 in) in head-and-body length and stands 48–56 cm (19–22 in) tall at the shoulder; females weigh around 5–12 kg (11–26 lb) while males weigh around 6–17 kg (13–37 lb).

The adult bobcat is 47.5 to 125 cm (18.7 to 49.2 in) long from the head to the base of its distinctive stubby tail, averaging 82.7 cm (32.6 in); the tail is 9 to 20 cm (3.5 to 7.9 in) long. Its "bobbed" appearance gives the species its name. An adult stands about 30 to 60 cm (12 to 24 in) at the shoulders.

Without a clearer image or a better sense of scale I cannot say which. Their silhouette is just too similar.


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Crow branch pecking behaviour
I was walking through a small park when two crows started cawing at me, and followed me, flying from tree-to-tree as I walked. I speculate that this is a territorial or protective behaviour, but what I found different was the crows were violently pecking the branches nearby them. I have no memories coming to mind of seeing this behaviour beforehand. I speculate that this behaviour could be threat displays, but a quick search on Google did not reveal to me any authoritative studies on this phenomenon. I'd appreciate more information and sources.

This question has been added as a casual observation on iNaturalist.

Anything like this? https://www.youtube.com/watch?v=rQZj59-Kufc

@theforestecologist That is strikingly similar.

This is a good question. This type of behavior -- pecking at a branch, wiping the side of the beak on a branch, pulling off twigs and dropping them, or knocking off pieces of bark -- is quite common among many corvid species, particularly when they are interrupted by something or someone that they might consider a threat. This includes not only potential predators but also potentially hostile conspecifics.
It is typically considered to be a form of displacement behavior. The concept of displacement behavior, from classical ethology, posits that when an animal experiences two conflicting drives to do two different things, it doesn't know which to do and does a third thing instead to dissipate the drive or anxiety. For branch-pecking in crows, see E.g Kilham and Waltermire 1990 Ch. 12.
Referece: Kilham, L., & Waltermire, J. (1990). The American crow and the common raven. Texas A&M University Press.

Sorry but I couldn't resist. It is certainly amusing that the answer comes from you (with the name corvus and a crow for DP)

Indeed - as the resident corvid I felt somewhat obliged to answer this question.


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Can a virophage potentially be used to cure a viral disease?
Wikipedia states "Virophages are satellite viruses that inhibit or impair the reproduction of the auxiliary virus."
Is it theoretically possible for a virophage that doesn't hurt the human body to attach itself to a more serious virus like the AIDS virus for example and be used to wipe out the virus, or at least inhibit it's reproduction?  I'm completely ignorant of the virophage relationship, so feel free to inform me as needed.

There are few enough virophages occurring in nature that I don't know if there's a clear and compelling case for them being potentially therapeutic.
In principle however, the answer is yes, though they may suffer from the same problems that bacteriophage treatments have suffered during their history - difficulty in preparation, extreme species specificity, and fairly daunting regulatory hurdles. While viral diseases don't have the "Or we could just use antibiotics, which work" out which made bacteriophages less popular, as far as I know there's not been a suggestion of widespread virophages against human pathogens.

In theory it should be possible, though this approach seems to be limited by the nature of the virophages known today. They seem to "infect" (this is actually wrong, since they take use of some of the proteins produced by the mama virus and do not infect these viruses) only very big DNA viruses.
This article (which is interesting to read in this context) talks about 400nm for the mimivirus, which is quite a lot. The problem is that many of the viruses which are interesting are fast mutating RNA viruses like HIV and the Ebola virus.


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How can I tell if a certain marker is useful to date a phylogeny?
If I have a phylogenetic tree for a genus, how can I tell if a certain protein would be a good phylogenetic marker to use if one wanted to use a molecular clock to date the age of some speciation event in that a genus? How can I look for it on a tree?

Speed of Sequence Divergence
You need to use a sequence which diverged only little among most closely related lineages in your tree and diverge quite a lot among most distantly related lineages. In other words, you need a sequence that diverge at a rate that is convenient for your needs.
If you investigate a young tree (a tree which MRCA of all lineages lived recently) you need a sequence that diverge quickly through time. If you investigate an "old tree" (a tree which MRCA of all lineages lived a long time ago) you need a sequence that diverge slowly through time.
Selection
Selection is affecting how fast two sequences diverge. But because selection is specific to the environment experienced by the individuals in each lineages, it can be more difficult to use sequences under selection as a molecular clock (exception of highly conserved selection which are under purifying selection used for very large trees). So we use neutral sequences.
Rate at which mutations fix
Let $u$ be the mutation rate for the sequence of interest and $N$ be the population size. The number of new mutations per year is equal to $2Nu$ (assuming a diploid population). Now, knowing that the sequence is not under selection, the probability of reaching a single mutation to fix (=to reach a frequency of 1 in the population) is $\frac{1}{2N}$ (see this post for a very introduction to why the probability of fixation is inversely proportional to $N$). As a consequence, the rate at which mutations fix is $2 N u \frac{1}{2N}=u$. In other words, the rate of mutation fixation is the mutation rate (for neutral sequences).
Rate at which mutations fix and sequences divergence
The term, sequence divergence is not clearly define. Typically, one would mean "average number of pairwise differences". Assuming that each new mutation that fixes occurred at a new locus (infinite allele model), then the number of pairwise differences between two lineages is the addition of the number of mutations that fixed in each lineage, that is $2u$. Always under the infinite allele model, the probability of the average number of pairwise differences to equal k is given by a Poisson distribution.
Wrapping up

how can I tell if a certain protein would be a good phylogenetic marker

The sequence

has to be neutral (it makes things easier)
has to have a mutation rate of the right order of magnitude (it improves accuracy of the estimate and therefore improves statistical power)


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Is designing alien life still just science fiction?
As we continue to search for life in very different environments than the earth, it would make sense to me to think about and design lifeforms (theoretical) that could work in these environments. I know that we are searching for life in extreme environments, but are we thinking about lifeforms that could have evolved in such environments? (Even if we dont find any)
The idea of the atom comes from ancient greek philosophers long before one could find any evidence for it. Although their views on what atoms look like and how they behave were incorrect, one could later refine this model through evidence and experimentation.
I think some good thought could makes us learn what to look for in the first place.
Is this still just a field that science fiction thinks about, or are there any serious publications on this topic? If not, why not?
Clarification: I mean the theoretical design of lifeforms. Not just manipulating and editing existing lifeforms, I mean designing completely new theoreticaly plausible lifeforms, within the constraints of a given environment. On paper or simulation etc, not actually making them physically.
If you find any scientific papers on how and what kind of life could exist for example on Titan, Europa, below Earths crust etc... or any other environment, please link to them in your answer. Thanks!

What is your definition of "new lifeforms"? You said without the use of existing life forms so you mean to synthesize a new strand of DNA as a genome (by selecting some genes you want to be present in the "new" organism"  and then let this grow or what?

No, I don't mean anything physical. Just thinking about what kind of life could exist.

First, you can check out this Wikipedia entry: Hypothetical Types of Biochemistry. I caution you that the scientific utility of many of these hypotheses isn't great since they are, at least currently, untestable.
Second, your question brought to mind some current research by two groups of scientists in the field of synthetic biology which may, in some way, answer your question. I will briefly mention these below.

Scientists are attempting to create synthetic organisms with minimal genomes (those in which every gene is essential). In one of the more recent studies (Hutchison CA, et al. 2016. Design and synthesis of a minimal bacterial genome. Science.), they randomly knocked out genes of an organism and then, based on survival and growth, classified them as essential, non-essential and quasi-essential (deletion results in growth impairment). They were then able to pare down the genome to 473 genes, which they claim "has a genome smaller than that of any autonomously replicating cell found in nature".
Important points from this research with respect to your question:

Of the 473 genes in the organism described above, 149 have an unknown function. In other words, we still have a limited understanding of what exactly is required for the basic biochemistry of life on Earth. To quote the article:

...biological functions could not be assigned for the ~31% of the genes... Nevertheless, potential homologs for a number of these were found in diverse organisms. Many of these genes probably encode universal proteins whose functions are yet to be characterized.

Additionally, before their knockout approach described above, the researchers attempted creating minimal genomes by rational design. Note that this is not designing new organisms but rather deleting genes from an existing genome based on whether they are thought to be essential. They failed. Quoting a press release (emphasis added):

[The researchers] initially formed two teams, each with the same task: using all available genomic knowledge to design a bacterial chromosome with the hypothetical minimum genome. Both proposals were then synthesized and transplanted into M. capricolum to see whether either would produce a viable organism.
  “The big news is we failed,” Venter says. “I was surprised.” Neither chromosome produced a living microbe. It's clear, Venter says, that “our current knowledge of biology is not sufficient to sit down and design a living organism and build it.”

In another avenue of research, scientists are attempting to create synthetic cells based on self-replicating RNA and compartmentalization by spontaneously forming fatty acid vesicles, perhaps somewhat plausibly mimicking how life may have arisen on Earth. Of interest to you may be this review (Blain and Szostak. 2014. Progress Toward Synthetic Cells. Annu Rev Biochem.) which, in their words:

[focuses] on bottom-up approaches to the construction of artiﬁcial cells from molecular components or subsystems. We do not discuss the top-down approach of systematically removing genes from extant organisms to achieve a minimal genome, nor do we consider the creation of new types of cells by genome synthesis or extensive genome editing.

They say in the article (emphasis added):

In vitro translation systems have successfully been incorporated into vesicles, resulting in the efﬁcient synthesis of proteins... However, replicating the entire system, including DNA and RNA polymerases, transcription and translation factors, transfer RNAs, the ribosome, and other components, is still a distant goal, and proposals to do so involve more than 100 genes. Properly coordinating the replication of such a large synthetic system may require additional regulatory components.

Take away message: We are not yet able to design or create, de novo, living organisms based on known biology, let alone organisms based on some hypothetical biology of another planet.

Interesting answer +1! But I just want to draw your attention to this line I mean the theoretical design of lifeforms. Not just manipulating and editing existing lifeforms, I mean designing completely new theoreticaly plausible lifeforms, within the constraints of a given environment. On paper or simulation etc, not actually making them physically. to which only your last paragraph seems relevant.

@another'Homosapien' Thanks. The point I was trying to get across is that people are trying to design synthetic life within the framework of known biochemistry. However, they haven't succeeded. Given that, how could we possibly design organisms with an entirely new and made up biochemistry for life on planets that we know almost nothing about?

Also, I want to emphasize that it is leading researchers in the field that are saying we don't possess the knowledge to design and build a living organism, and the ability to do so is far away.

The answer to this question can go as far as anybody's imaginations. So I'll just tell why the answer is what it is, and try to include scientific facts (possibly with references) wherever possible.
Simple Answer: Designing alien life forms on the basis of current theoretical and practical knowledge of science (if this is what you mean) is still, and seems to remain, a field of science fiction only.
Why? Because, simply, the proposed organisms can be unlimited. Even if this field matures as a science, it will remain as large as the universe itself, because there are literally no boundaries and limitations to speculation and imagination. Only recently have researchers agreed that discovering organisms similar to humans is much much less likely than any layman thinks. Actually, there is even a formula for it, known as the Drake equation after Frank Drake who proposed it. The equation is:
$N = R^* \times f_p \times n_e \times f_l \times f_i \times f_c \times L$
where:

$R^* =$ the average rate of star formation in our galaxy
$f_p =$ the fraction of formed stars that have planets
$n_e =$ the average number of planets per star that can potentially support life
$f_l =$ the fraction of those planets, fl, that actually develop life
$f_i =$ the fraction of planets bearing life on which intelligent, civilized life has developed
$f_c =$ the fraction of these civilizations that have developed communications i.e. technologies that release detectable signs into space
$L =$ the length of time over which such civilizations release detectable signals

Obviously, this answer comes out to be very small, meaning that intelligent life is very difficult to find. But that doesn't mean finding life is difficult. And this claim gets even more support when scientists find water on mars and even mercury! Now, to give a bit of knowledge, this field is not really limitless; there are (at least) two limits (i.e. I'm not including more). The first limit is source of liquid water$^*$. Now, knowing that water is easy to be found almost anywhere, this does not seem quite a difficult one. Another one is source of energy. Now this is a difficult one. The problem with discovering life (in near future at least) is the area in which we are searching. Most of the searches (by telescopes of course) are being conducted near red dwarf stars. There are quite some reasons for it:

red dwarf stars are quite stable
they have very long life
they are pretty less shiny (making observations easier)
they may be home for many super-Earths

But being less shiny also poses a problem: too little energy for life. Red dwarf stars emit most of their radiation in the infrared portion of spectrum, which is pretty useless for plants (on Earth at least). Now, to survive in a red dwarf system, plants need to capture infrared light. Thus, the speculated plants in red dwarf systems will be pitch black just to absorb more energy. Also, red dwarf stars are pretty lightweight, as less as 7.5% of sun. This means they have less gravitational pull i.e. they will have much lighter planets in their Goldilocks zone. Now, much lighter planets means much less gravity on planet's surface. Thus, the speculated plants in red dwarf systems will be a lot higher than plants on Earth. But, less gravity also means much less density of air even on surface. Now, you can interpret it yourself. And, not just to surprise you, there would be absolutely no surprise if in future a satellite discovers silicon-based life, because it is really possible for life to emerge from silicon instead of carbon!
$^*$why I am continuously saying liquid water has a reason. Water is actually one of the very few candidates that can serve the purpose of maintaining life forms. Its one of a handful of liquids which are liquids at desired temperature. As one might think, life cannot survive below a certain temperature, simply because below that temperature, the liquid itself would absorb all the metabolic heat from organism and evaporate. So, it is quite relevant to say liquid water here.
What I meant to say is that there are technically no boundations to designing alien life forms, as long as you talk about the whole universe. So, this does not really count as science. After all, if you search science definition on Google, you get this:

the intellectual and practical activity encompassing the systematic study of the structure and behaviour of the physical and natural world through observation and experiment.

This does not include imagining alien life forms in any way. So, I do not think this subject would ever be considered as scientific by the scientific community. Mostly, scientists are not indulged in this kind of work because they like to observe and interpret natural phenomena rather than imagining them. Scientists make laws from nature rather than applying laws on nature. Still, there are some scientists who take this matter seriously and publish scientific papers about it. I could find only one (PDF) related to this point. You might get some more on the internet.
In the end, if you think about how plants would look on a planet in a red dwarf system, you might end up with this:

Bonus: Dawn space probe from NASA has detected organic materials on Ceres(!) Now, what kind of organisms would you expect to see there based on our current knowledge about Ceres?

"What I meant to say is that there are technically no boundations to designing alien life forms, as long as you talk about the whole universe". However if you consider only one environment (for example the moon Titan) you already get a lot of limitations. Do you know of any scientific papers that consider these limitations and try to come up with various possible lifeforms that could survive in such an environment? (Also note that you don't absolutely need water for life, you probably just need some kind of solvent that behaves in a similar fashion)

Why are scientists not interested in these things? This seems rather odd. If you find any good scientific papers please add them to your answer.

Thank you for a good answer. I will award the bounty to the best answer at the end of the period. I am very interested in this and the more diversity I can get with different answers the better.

Is there a biological field for designing life?

The field is called synthetic biology. It is a very new field. With not many player. Currently being constructed is a synthetic yeast Sc2.0. There is attempts to get interest and funding for a synthetic mammalian genome. The synthetic human genome HGP-Write.
More serious work is adapting life to do something. Stuff that we are more familiar with like GM crops. De horned cattle. Better race horses.  etc

There is also some cool research designing life forms that use synthetic de nova nucleotides (so non-A,C,G,T or U). http://www.pnas.org/content/114/6/1317.abstract


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number of RNA pol II molecules in a given human nucleus?
Does anybody have any estimate on the number of RNA pol II molecules in the nucleus of a given human cell? For example, how many RNA polymerase type II protein complexes would there be on average at a given time in, say, a human immortalized lymphoblastoid cell line (LCL)?

it is highly variable even in a single cell type.
Dont know for a human cell but this is the range for ecoli: 1500-11400
check this site out. got this number from there (its quite useful for questions like these):
http://bionumbers.hms.harvard.edu/bionumber.aspx?&id=101440&ver=3&trm=RNA%20polymerase
You can estimate protein copy numbers and there are techniques available for doing so. One of such techniques:
http://www.mcponline.org/content/11/3/O111.009613.long
You can also calculate concentration using traditional techniques like western blot and elisa and calculate approximate copy-numbers (you have to also calculate average cell volume and number of cells for protein extraction.


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what are hyperbranched amplicons in DNA sequencing?
I am reading an article about single-cell sequencing:
http://www.nature.com/nbt/journal/vaop/ncurrent/full/nbt.2720.html
And came across the concept of "hyperbranched amplicons". I googled for it but don't get much luck. The best I could find is it mentioned in another single-cell sequencing method here:
http://en.wikipedia.org/wiki/Multiple_displacement_amplification
Can someone give me a definition for it?


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can the face of a person be accurately predicted from DNA information?
http://blogs.smithsonianmag.com/artscience/2013/05/creepy-or-cool-portraits-derived-from-the-dna-in-hair-and-gum-found-in-public-places/?utm_source=plus.google.com&utm_medium=socialmedia&utm_campaign=20130503&utm_content=collageartdna
Can the face of a person be accurately rendered just from analysing a DNA sample of that individual?

I posed a similar question a while back. You might want to check it out, even if the answer is inconclusive...

Not accurately. Assuming the DNA information is the DNA sequence, you can't tell which genes are being expressed and which are being silenced. These are through chemical groups on the DNA which aren't generally picked up.
Also there's the environment that grossly affects what you look like, how much you weigh, your skin colour and cosmetic surgery.

Just for added clarity, the chemical modifications I referred to were epigenetic mechanisms of methylation and histone acetylation etc.

Just saying grossly means net-gain. It's used when describing things like financial matters, and really doesn't make sense here..unless you mean they've had some sort of terrible accident :P

@Starkers in medical terms it means that which is visible to the naked eye. It also is used for financial matters. It's a homonym.

@Starkers Gross Anatomy... It's probably not a bad idea to assume someone knows something you don't until you can prove them incorrect.

It depends what you mean by "predict". Consider that the faces on genetically identical individuals, such as identical twins, are very similar, even in old age. If you look at the processes of development over the life of an individual as a more-or-less deterministic and predictable phenomenon, then you might argue that faces are predictable from DNA info. The fact that no one has ever done this from first principles is another issue - in principle it is possible.

So you are saying it is possible to analyze someone's DNA and determine approximately what their face will look like?

I'm saying that if "nature" can reliably produce similar-looking faces from similar DNA, then there is an underlying mechanism operating which is accessible to scientific investigation, possibly leading to a technology of predicting facial features by examining a person's genome. But not yet.

That's cool. It would/will be interesting to see what comes of that in the coming years. Thank you for sharing :)


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Creative ways to deactivate alpha-amylase taken from fungi
I can deactivate $\alpha$-amylase in ways such as extreme temperature controls, pH controls of the solution it stays in, or adding salt to the solution.
However, are there any other unique or elaborate ways to deactivate the enzyme? (maybe the lock-and-key hypothesis also works for enzymes AND enzymes?)

Amylase inhibitors have attracted much attention because of their potential in treating type 2 diabetes.
You can inactivate most enzymes by using a specific inhibitor. One class of inhibitors consists of molecules that resemble the substrate molecules but are not acted upon in the same way. These will bind to the active site and will prevent the substrate from binding. An inhibitor of many amylases is acarbose. This is a competitive inhibitor which means that inhibition is overcome by high concentrations of substrate.
And if that isn't enough to get you started here is an entire thesis on the topic of amylase inhibitors.
If you want to permanently block activity the ideal compound would be one which binds to and covalently modifies the active site, destroying enzyme activity. This would be an irreversible inhibitor. I haven't been able to find a reference to such a compound however.

So, to conclude, does 'enzyme deactivation' simply means 'deforming its active site'? Since both denaturation and using inhibitors basically mean destroying the enzyme active sites.

@Greek Fellows - in fact I almost commented upon your choice of "deactivate". In the context of your question I think that "inactivate" is what you mean. To me the word "deactivate" implies that there is a corresponding activation process - so for example an enzyme might be activated by phosphorylation then deactivated by a phosphatase. Also most enzyme inhibitors don't destroy the active site - they block it by competing for binding.

yeah, I should have been careful about the wording...


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The real definition of carbohydrates
Carbohydrates are often defined as compounds with only C, H, and O and the H and usually the O atoms are in a 2:1 ratio.
Exceptions like deoxyribose exist, but why is it recognized as a carbohydrate?
What distinguishes a carbohydrate from other compounds?

The definition of carbohydrates as compounds containing $C$, $H$ and $O$ usually with the empirical formula ${C_m(H_2O)_n}$, is outdated.
More rigorous and a accurate definition would be Polyhydroxy Aldehydes and Ketones composed of Carbon, Hydrogen and Oxygen. Moreover, the nomenclature including Mono-, Di-, Oligo- and Poly- "Saccharide" is preferred over the now obsolete and too-general term "carbohydrate", since the etymological origin of the word "carbohydrate" is from the greek words Carbo- for carbon and hydor- for water which indicates that the carbohydrates are "hydrates" of carbon and have the empirical formula ${C_m(H_2O)_n}$, which is not always true. Instead "saccharide" is derived from the greek word for "sugar" and hence is much more accurate as it does not limit the definition to any empirical formula.
Apart from the polyhydroxy aldehyde or ketone characteristic of carbohydrate, they have a marked structural and functional variation from other biomolecules. This includes the absence of $S$ (as in proteins), $P$ and $N$ (as in proteins and nucleic acids), presence of Glycosidic bond (as compared to peptide bond in proteins, phosphodiester bond in nucleic acid, and ester linkages in fats or glycerides) and much greater structural uniformity as compared to other biomolecules.However, these characteristics are not absolute as is evident from the fact that several monosaccharide derivatives do contain $S$ or $N$ atoms. Actually, the entire group of amino-sugars (Hexosamines etc.) are usually classified under carbohydrates since they are primarily monosaccharide derivatives obtained through enzymatic amination.
These characteristics distinguish this class of compounds without having to assign a empirical formula to it.
ADDENDUM
Adding the clause compounds which can, on simple hydrolysis yield polyhydroxy aldehyde or ketones in the definition helps involve certain non-reducing sugars like Sucrose.

Nice summary, but haven't you gone a bit far with the "absence of..." section? What, for example, would you classify N-acetyl glucosamine as? Or isopropylthio D galactoside? These are derivatives of saccharides containg N and S respectively, and it makes no sense to not classify them, broadly speaking, with their parent molecules.

@AlanBoyd The absence is not absolute and I forgot to mention that(corrected). However, the compounds you mention are referred to as monosaccharide-derivatives and not monosaccharides as such. These derivatives, usually cannot be classified into one of the traditional groupings which are not defined by strict structural criteria. Broadly speaking they are carbohydrates (i.e. monosaccharides) but while distinguishing, omitting a few exceptions might help us grasp the uniqueness of each group and I guess is what the asker meant with "What distinguishes a..?".

@SatwikPasani That's exactly what I meant. Thank you for this rather slick summary - very clever to limit the composition with C, H and O.

@TomD The addendum tries to resolve this problem.


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Method to inject genes into cells
The famous Hershey and Chase Experiment uses phages to inject genes into cells.
In the beginning, Professor Yamanaka injected 24 types of genes into cells to figure out which genes turn a cell into ES cells.
Did he also use phages?

Remember, phages infect bacteria. It looks like he used something called pMXs-based retroviral vectors instead, which is based on the Moloney murine leukemia virus (MMLV).
I have never heard of that virus before, but I do know of others used in vivo to deliver genes, including Lentivirus, Adenovirus, and Adeno-associated virus. All have their strengths and weaknesses. Adenovirus is large so you can fit a big gene inside it, but it tends to illicit a high immune response. AAV, on the other hand, is very small but has a much more mild immune response. It can fit a gene about 4kb long inside or half that if you use a fast expressing form called self-complementary AAV. What is nice about AAV is one of the subtypes (technically callled serotype) can cross the blood brain barrier, so it has already been used in clinical trials to try and treat neurological diseases, including Parkinson’s.

+1. You will want to note the methods section the linked paper entitled "Retroviral Infection." The pMX vectors were used to make the retrovirus, which was used to deliver genes to the cells, which were selected for using G418 (an antibiotic). You may want look into transfection and transduction.


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How can epigenetic changes be erased if they are inherited?
I’m a little bit confused about DNA methlyation reprogramming and about the nature of an epigenetic phenomenon. According to Wikipedia:

After fertilization the paternal and maternal genomes are once again demethylated and remethylated (except for differentially methylated regions associated with imprinted genes). This reprogramming is likely required for totipotency of the newly formed embryo and erasure of acquired epigenetic changes.

I don't understand how something can be thought to be both heritable and erasable. Any help would be greatly appreciated.

I'm voting to close this question as off-topic because the poster has already answered the biological question by his own research, for which he is to be commended. He can find the origin of the term in a similar way, but that is not biology.

@David Are you kidding? There is a terminology tag on this website. Maybe I should have use it, but I don't think my question deserves to be closed for that.

The tags that people use do not define the purpose of this site or the acceptability of questions. This is explained in the Help on Asking questions. Questions on why something has such and such a name are generally of little interest to biology, except for its history, and, in any case you show no evidence of trying to find definitions yourself. A Google search for "Epigenetics Definition" includes a definition by Robin Holliday that might remove the unstated and erroneous assumption of your own on the meaning of the word.

@David - there is definitely important misunderstanding still present in the question that was not addressed by the OP, and it seems this is a misunderstanding you have as well. I see absolutely no reason to close this question, because even if its title seems to be about semantics an appropriate answer would not need to be.

@David All the websites and sources I used before posting this question mentioned that "Epigenetics is the study of heritable changes in gene function that do not involve changes in the DNA sequence." (This comes from the wikipedia article about epigenetics, but this isn't the only source that mentions the heritable character of epigenetics phenomena). I know that we are supposed to make some efforts before asking anything here, and that's what I did. Unfortunately, I didn't find your Robin Holliday definition before, so sorry about that. In all cases, I still think my question matters.

@BryanKrause — It is not just the title that is about semantics, it is the concluding sentence in the question, clearly meant as the key question because it is in bold. There may be interesting answers on epigenetics, but they need a clear biological question first. This is not.

@David The answer is because some portion of epigenetic changes are indeed heritable. How would you propose the questioner reframe their question to fit your narrow view of what makes a good question here? Their curiosity is clearly based on the biology of the situation. SE English language and usage is not for scientific terminology.

(1942) "Biology. of or relating to epigenesis, or the successive differentiation of undifferentiated cells in an embryo." This just illustrates that words are coined, used in different contexts, get contorted in the public mind by political and religious misuse (Lysenko, anyone?), but that most English-speaking professional scientists manage to live with their scientific usage, understanding what they mean. The structure of a compound word coined in German, for example, is clear to German speakers. English speakers often neither know or care about the structure of words from Greek or Latin.

@David I don't understand the point of your last comment, but I'm not a professional scientist (still a student), and my mother tongue isn't English either, so sorry again about all that mess. Anyway, I don't really see how to improve my question. What I don't understand is that epigenetics phenomena are supposed to be heritable, while apparently those changes are erased after fertilization... which doesn't make sense to me. I don't really care about the origin of the word "epigenetics", I just would like to understand how changes can be inherited and erased at the same time.

@BryanKrause — Not nice, saying that I have a narrow view on the suitability of questions. I not only exercised my right/duty to maintain the standards of the site, but explained to the poster my reasons for doing so, something I am not obliged to do. I refered the poster to the SE Help, as the source of information on posting good questions, and told him how to find the origin of the word himself, together with naming a SE site that is more appropriate — SE EL&U does take questions on technical English.

OK. If that's your question, I'll edit it in that direction. Perhaps @BryanKrause will add further, and then I'll withdraw my close vote.

@David Thanks for editing it. I just made it "sound" a little bit more like I would have written it. Hope you don't mind. :)

I have done a presentation in epigenetics and the main topic was imprinting.
This paper will answer all your questions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941233/
I am adding some glimpses from this  paper here
Mammals are diploid organisms whose cells possess two
matched sets of chromosomes, one inherited from the mother
and one from the father. Thus, mammals have two copies of
every gene. Normally both the maternal and paternal copy of
each gene has the same potential to be active in any cell.
Genomic imprinting is an epigenetic mechanism that changes
this potential because it restricts the expression of a gene to
one of the two parental chromosomes. It is a phenomenon
displayed by only a few hundred of the approximately 25,000
genes in our genome, the majority being expressed equally
when inherited from either parent. Genomic imprinting affects
both male and female offspring and is, therefore, a consequence
of parental inheritance, not of sex. As an example of
what is meant by this, an imprinted gene that is active on a
maternally inherited chromosome will be active on the maternal
chromosome and silent on the paternal chromosome in
all males and females.
Hope this help and please ask if you do not understand the paper.Thank you


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How does vitamin C increase iron uptake?
I've read that vitamin C increases the iron uptake in the human body. How does that work, physiologically?

Vitamin C both enhances iron uptake, and affects iron metabolism:

in addition to the known ability of dietary ascorbate to enhance nonheme iron absorption in the gut, ascorbate within mammalian systems can regulate cellular iron uptake and metabolism. Ascorbate modulates iron metabolism by stimulating ferritin synthesis, inhibiting lysosomal ferritin degradation, and decreasing cellular iron efflux. ... Importantly, this iron-uptake pathway is of particular relevance to astrocyte brain iron metabolism and tissue iron loading in disorders such as hereditary hemochromatosis and β-thalassemia. Recent evidence also indicates that ascorbate is a novel modulator of the classical transferrin-iron uptake pathway, which provides almost all iron for cellular demands and erythropoiesis under physiological conditions.

--The active role of vitamin C in mammalian iron metabolism: much more than just enhanced iron absorption!

stimulating ferritin synthesis, inhibiting lysosomal ferritin degradation, and decreasing cellular iron efflux. Is it possible to translate these 3 things into simpler language?

Just v various ways of increasing iron metabolism: Making more of the handling proteins, preventing them from being broken down, and keeping iron in the cell


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Does any lifeforms can make a haploid cell from any other cell without meiosis?
Like the title says, is it possible to produce haploid cells without meiosis?

I don't think so, but it is possible to transfer the nucleus of a haploid cell to the body of a diploid cell and vice versa

The question is a bit unclear

Can you produce haploid cells without meiosis?

The question is a bit unclear. for two reasons

What do you mean by "you". You mean can we do such thing with modern technology or do you mean does it ever happen or do you does it ever happen in human cells.
It is also unclear what from. Are you implicitly asking whether "you" (whatever 'you' mean in your sentence) can make a haploid cell from a diploid cell or form anything?

Answer
In this answer, I will assume that the question is

Does any lifeforms can make a haploid cell from any other cell without meiosis?

The answer is yes. Many organisms have a long haploid stage during which many mitosis occur. Haploid cells undergoing mitosis results into two haploid cells.
You might want to read more about life-cycle (wikipedia), especially the sections on haplontic life-cycles and haplo-diplontic life cycles.

I think these are great answers that will cover OP's curiosity, but the question isn't really up to our standards - can you edit the original question to fit your answer?

Thanks for your answer. English isn't my mother-tongue, but you assumed the question correct Remi. I had a lecture about Saccharomyces cerevisiae, and wasn't sure if the budding generates haploid cells. But if I understood it correct, an "a" mating type spore can generate a haploid "alpha" cell without meisosis, right?


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If hands are folded with both index fingers parallel, they will come closer and touch eventually?
I have a question out of curiosity. It is just something I found out/discovered:
if I fold my hands into each and let my two index fingers (see picture) be in parallel then they will eventually come closer to each other and touch.
How can this be explained?

Another thing I found out: if I fold my fingers on my left hand slightly and then with my right hand squeeze the wrist of my left hand (see picture), then the fingers of the left hand will fold more and more. Is this a coincidence of general?

The easy way to explai the first phenomenon is that at rest, your fingers - all of them - curl. Relax on your bed on your back. No matter what direction your hands face, they will curl inward as if loosely holding an egg. That's the anatominal position of the hands at rest, because the finger flexors are stronger than the extendors. So once you set the finfers up, you'll tire of keeping them extended, they'll start  to relax, and in doing so, will tough.
If I'm understanding the second example, that's because the flexor tendons for your fingers are actually in your forearm. Squeeze them and it shortens the tendons causing flexion.

the explanation for the first picture is that this is due to an invisible attraction force which is called (Ideomotor effect) which affects on the left lobe of the brain which permits to our muscles to move involuntary and unawareness.So they will come closer as if they are like a magnet and a nail.


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Why do we exhale after we hold our breath?
I tested this out with my friends, and I find that after they hold their breath and can't hold it anymore, they exhale air, instead of inhaling air.
Interestingly, they all try to inhale in as much air as possible before starting to hold their breath. When I told them to exhale as much air as possible before starting to hold their breath, they inhaled air after they can't hold it anymore.
It's understandable that when one exhales then holds his breath, he needs air and thus he inhales afterwards. But when one inhales then holds his breath, shouldn't he inhale again after "using up all that air he inhaled before holding hi breath"?

The lungs are not consuming the air as such, they are just adding a Carbon element to the O2 in it.

@HermannIngjaldsson ??? I thought CO2 was the by-product of cellular respiration.

O2->CO2 is what the lungs do with the air you give them.

@HermannIngjaldsson um.. could you be more specific? I don't think the lungs convert O2 to CO2; it should be the cells throughout the body that uses O2 and produces CO2, which is sent out from the blood into the lungs. Or do you mean the conversion of O2 to CO2 in the cells of lungs?

you breathe in air, which contains that necessary thing, oxygen. and you breath out that same air, just then a bit of the oxygen has been combined with a carbon atom. the cells throughout the body take o2 and give back co2, its just that the lungs take care of extracting that necessary o2 out of the air for them.

@HermannIngjaldsson ah, I see.

Try maximally exhaling, and then hold your breath. ;)

@HermannIngjaldsson I think that's a very limited and confusing way to describe it, especially the first two comments.  Your statements suggest that C is added to O2 in the lungs which is not the case.  The lungs are purely a gas exchange organ in this sense.  O2 is brought in, CO2 kicked out, following concentration gradients.  The air you breath in is not the same as you breath out.

This is more about basic physics than biology. When you hold your breath, you normally take in one last long breath and keep it in as long as possible, Your lungs are therefore already full of gas (remember that the oxygen used by our lungs is only ~22% of the total volume of air you inhale). Therefore, when you release that breath and want to take in a new one you need to first empty your lungs out in order to refill them.
In addition, you need to have your lungs empty in order to be able to expand them and draw in more air. There is no biological reason for any of this, it is the same principle as trying to use a turkey baster:

If you use it once and pull up some liquid into it, you will have to let air out before you can use it again. Your lungs work in the same way. Test this by exhaling all the air from your lungs and then holding your breath without inhaling. When you want to start breathing again, you'll be able to breathe directly in without needing to exhale first.

Good question.
If you inhale on top of inhaled air this is more work. There is more dead air, air which is not as useful due to the lower concentration gradient. And we breathe more to exhale carbon dioxide than we require oxygen. Low oxygen levels only push us to breathe when oxygen levels are a good deal lower, however tiny changes in carbon dioxide causes changes in our ventilation rate almost immediately.
It is also more work as our muscles require more energy to inflate an already inflated chest. This is the case in COPD patients. Try this: take a deep breath in and now holding that air in, breathe normally on top of that air. Feel how difficult it is and how breathless you feel.

It's understandable that when one exhales then holds his breath, he needs air and thus he inhales afterwards. But when one inhales then holds his breath, shouldn't he inhale again after "using up all that air he inhaled before holding hi breath"?

Before we hold our breathe we first inhale some air inside.
So, after holding it for some times, carbondioxide (CO2) which can be toxic to our body will be released after completing metabolic processes inside our body which will be pushed to our thorax, ready to be expelled.
The partial pressure of this gas (pCO2), is the primary fast (minutes or hours) trigger for breath; where partial pressure of Oxygen (pO2) is a slow trigger (hours or days). This explains why patients with severe re-acutized cronic obstructive pulmonary disease (COPD) stop spontaneous breathing, even if their pO2 falls, because of augmented pCO2.
The pCO2 is sensed in the human body in the Central Nervous System (CNS), precisely in the ponto-bulbar centers of breathing. The pO2 is sensed at periferical strucrures as the glomi aorticus and carotideus.

Welcome to the site! While you may have the beginnings of a good answer, it is trapped inside of a gigantic run-on sentence with several misspellings and run-together words that make it very difficult to determine what exactly you're trying to say. Please [edit] your answer to improve it, highlighting your answer to the question and not just giving a review of the mechanics of breathing, which isn't really relevant.


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Are females more flexible than males in all mammals?
It's common that human females have a more flexible body than males, (but I don't know why, so it'd be helpful if someone answers why so as well!) but does this apply to all mammals?

In which terms more flexible?

You mean physically flexible ?

Do you mean plasticity? Devlopmental plasticity?

Try birthing a child for once. You need to be flexible to accommodate the growth of another organism inside you.
Take a look at some pictures of the mothers spine during the course of a pregnancy, you will have no further questions. Same with belly size, breast size and vagina size upon birth.
This video is a nice explanation of this. Also includes the different centers of gravity for males and females (human).
http://www.youtube.com/watch?v=WO8DtsZO1nA

This might be true for spinal flexibility, I'm not sure it tells the whole story. Men are almost always stronger than women of the same size, and I'd be surprised if this isn't related to flexibility. Perhaps women pay for their increased flexibility with reduced strength?

Males and females are more similar in most other mammals (with some spectacular exceptions where males compete strongly for females and have evolved weaponry to help them). When your life is threatened every day and you survive by running and fighting, there is a strong evolutionary incentive for both sexes to converge on a single optimal body shape.

@DisplayName yes, I find that the spine curve gets very intense during pregnancy.


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Bacterial capsule vs. slime wall
I've read that the bacterial capsule protects the bacterium from phagocytes and prevents water (and nutrients, possibly?) leakage from the bacterium.
A less organized and less dense version is called a slime layer. It seems that the slime layer has similar functions, according to Wikipedia.
What are the differences between the effects a capsule and a slime layer bring to a bacterium?
I thought about the followings:

The capsule covers most part of the bacterium, so adhesion proteins and transport proteins on the plasma membrane do not work effectively, whereäs with a slime layer, more proteins on the plasma membrane are exposed to the exterior, making them work more effectively.
Maintenance of the capsule takes more energy than that of the slime layer simply because there are more glycoproteins in the capsule.
Bacteria with capsules are less likely to lyse than those with slime layers.

Is there anything else significant that goes on this list? Or are there any points I made that are not true?

According to the Wikipedia section on bacterial capsules, they're made of the same thing:

When the amorphous viscid secretion (that makes up the capsule) diffuses into the surrounding medium and remains as a loose undemarcated secretion, it is known as slime layer.

Todar's Online Textbook of Bacteriology synonymizes "slime layer" and "biofilm":

A true capsule is a discrete detectable layer of polysaccharides deposited outside the cell wall. A less discrete structure or matrix which embeds the cells is a called a slime layer or a biofilm.

This makes sense with what I remember learning about slime walls--the main difference I saw was that the capsule was directly associated with/only protects a single bacterial cell, whereas the slime layer is associated with/protects multiple bacteria. I'm not sure that I'd call it a biofilm though, as those are notoriously difficult to remove; their removal in hospital and food processing sysyems is a current research topic.
Regarding your three points above, I might instead argue that the slime layer provides another layer of protection in addition to the bacterial capsule.

So the slime layer protects multiple bacteria attached to each other due to the polar polysaccharides? If so, is this protection weaker than that of the capsule? Also, I don't understand how the polysaccharides can "diffuse into the surrounding medium". I thought the capsule / slime layer is the network formed by the polysaccharide parts of plasma membrane glycoproteins. How do these polysaccharides detach from their protein parts and diffuse into the surroundings? Or is it just that the polysaccharides have polar attractions with water (and possibly other polar substances)?

From Wikipedia: "The capsule... is a polysaccharide layer that lies outside the cell envelope of bacteria... which can be found in both Gram-negative bacteria and Gram-positive bacteria should not be confused with the second lipid membrane (or bacterial outer membrane), which contains lipopolysaccharides and lipoproteins and is found only in Gram-negative bacteria.

So the capsule is not a network of polysaccharides of membrane glycoproteins but simply a network of polysaccharides.


text:
Which phylum appeared most recently
I'm aware that our earliest records of many major animal and plant phyla come from the Cambrian or Precambrian periods, and I'm also vaguely aware of some of the objections raised with general concept of phyla. With this in mind, I'm curious which of widely accepted biological phyla appeared most recently, and what evidence do we have of their relatively recent appearance?
I'm most interested in animals, but I'd also welcome any information about other organisms.

In my view, we simply don't have good enough data to answer this question. The fossil evidence is too sparse prior to the Cambrian and the evidence that we do have suggests that the phyla were already too separated. Meanwhile, the depth of time and the different lifecycles and circumstances of the species involved mean that any "genetic clocks" we might use are likely to be too poor at keeping time and, indeed, different attempts have delivered different estimates of the time of divergence.

Can you give an example of a widely accepted phylum which is itself a member another phylum (according to phylogenetic analysis)?

Actually, I've decided I was wrong about most phyla being clearly paraphyletic. I think it's true, but we don't have the direct evidence needed for many phyla. The Echiura and Spinuncula group inside the Annelida.

As far as I know there is no phylum which appeared after the Cambrian. Every discussion beyond that is close to speculation, as the divergence estimates of different studies vary significantly.
You might want to look into one of the resources mentioned below:

http://www.timetree.org/index.php
http://www.onezoom.org/

I didn't mean for my question to be exclude the Cambrian from consideration. If it's true that all phyla appeared during or before the Cambrian, I'd still like to know which phylum appears latest in the Cambrian.


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Volvox Cellular Reintegration
A couple of days ago, I answered this question over on worldbuilding.SE with some information about volvoxes, and commenter Liam Proven pointed out that one of the claims I made was dubious.
I had first read about the volvox in a book that described their basic biology and life cycle (the book may have been Flatterland by Ian Stewart, but I no longer have a copy to verify). One detail I vaguely remembered was that since volvoxes are essentially colonial organisms, individual cells do not immediately die when the volvox disintegrates, but rather some of these cells can rejoin the cytoplasmic matrix of other colonies, similar to sponges.
Now, I read this a long time ago, and my memory is admittedly foggy, and I never had any university-level training in biology. It's entirely possible I'm conflating this with something completely different I read elsewhere, so Liam's comment sent me searching for more info.  And even if I am remembering correctly what I had read, it's possible the original author was mistaken.
The best article I could find on the topic was Cytoplasmic Bridges in Volvox and Its Relatives by Hoops, Nishii, and Kirk, but it doesn't appear to support my recollection (it talks mostly about the inversion process in embryos).
So I thought I'd bring the question to a wider audience. Do individual volvox cells reintegrate after disintegration, or do the mother's cells simply die?


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How do you merge SNP data with a reference genome?
My Data
I have a 23andMe file listing SNPs in the form:
rsid       chromosome      position        genotype
rsXXXXX         1           PPPPPP          CT
rsXXXXX         1           PPPPPP          GG

Fields are TAB-separated and each line corresponds to a single SNP. For each SNP, four fields of data are supplied.

An identifier (an rsid or an internal id)
Its location on the reference genome.

The chromosome it is located on.
The position within the chromosome is is located on.

The genotype call oriented with respect to the plus strand on the human reference sequence.

The reference genome is the human assembly build 37 (also known as Annotation Release 104).
My Question
How do I merge the SNPs into the reference genome?
For example, take the first line in my SNP file:
rsXXXXX        1           PPPPPP          CT
Part 1
I can see that I need to replace the nucleotide at position PPPPPP on chomosome 1 of the reference genome with a nucleotide from the genotype field, but which nucleotide am I supposed to use? C or T? And why?
Part 2
Where am I supposed to start counting from on the reference genome? Looking at chromosome 1 of the human assembly build 37, the first ~10,000 characters (excluding the first line description) are N. Is the first N number 1? eg. If PPPPPP was 100,000 would I replace the 100,000th character in the reference genome with the correct nucleotide from Part 1 of this question? Or should I start counting from the first non-N character in the fasta file?

First, you need to know which genome sequence does the SNP file refer to. They must have mentioned the reference sequence that they used.
As others mentioned the case of CT is heterozygosity. If you just want to mark the changes then discard the residue that is already present in the reference genome and use the other allele. However, you want to keep a track of the haplotype then you have make sure that a set of SNPs come from the same chromatid. This is difficult- you might still be able to know it for SNPs that are close enough to be mapped by a single read but it is almost impossible for SNPs that are separated well enough.
As Endre said, you have to start from the first nucleotide. However, it seems dubious that you are getting $\ (NNNN)_n$ in the beginning of chromosome 1. Complete assembled chromosomes do not have such stretches. Below are the first 10 lines of the chromosome 1 fasta file. See for yourself.
>gi|568815364|ref|NT_077402.3| Homo sapiens chromosome 1 genomic scaffold, GRCh38 Primary Assembly HSCHR1_CTG1
TAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAAC
CCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCAACCCTAACCCTAACCCTAACCCTAACCCTAA
CCCTAACCCCTAACCCTAACCCTAACCCTAACCCTAACCTAACCCTAACCCTAACCCTAACCCTAACCCT
AACCCTAACCCTAACCCTAACCCCTAACCCTAACCCTAAACCCTAAACCCTAACCCTAACCCTAACCCTA
ACCCTAACCCCAACCCCAACCCCAACCCCAACCCCAACCCCAACCCTAACCCCTAACCCTAACCCTAACC
CTACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCCTAACCCCTAACCCTAACCCTAACCCTA
ACCCTAACCCTAACCCTAACCCCTAACCCTAACCCTAACCCTAACCCTCGCGGTACCCTCAGCCGGCCCG
CCCGCCCGGGTCTGACCTGAGGAGAACTGTGCTCCGCCTTCAGAGTACCACCGAAATCTGTGCAGAGGAC
AACGCAGCTCCGCCCTCGCGGTGCTCTCCGGGTCTGTGCTGAGGAGAACGCAACTCCGCCGTTGCAAAGG

How to replace $N^{th}$ residue is quite a straightforward task. But that is a programming question and not the scope of this forum. Assuming that you have solved the part 1 problem and have a tab separated sorted file like this:
chromosome  position    residue
 1           79989           G
 1           100232          T
 3           341342          A

This script may not be the best but would work in a linux/*nix/Cygwin terminal, to replace the residues (ensure that you have gawk version >=4.0):
gawk -F "\t" '(FNR==1){x++} (x==1){a[$1][$2]=$3;next} (x==2){if($0~/>/){h=$0;sub(/^.*chromosome /,"",h);sub(/ .*/,"",h)} else{seq[h]=seq[h]$0}} END{for(i in a){s=0; for(j in a[i]){m=m substr(seq[i],s,j-1) a[i][j];s=j+1} m=m substr(seq[i],s); print ">Chr"i"\n"m}}' SNP_file Genome.fa | fold -w 60

Unfortunately I cannot explain how the script works, in this forum

"TAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAAC" blats to position 10,000 according to UCSC.  And look at it, as I said, it's repetitive and awful.  The OP just has a masked sequence.

Hmm.. yes.. I didn't notice that.. nonetheless the start is from the residue#1..

Genetics 101, you have 2 copies of all your DNA at every position, one copy from your mother, one from your father.  So for the "CT" one, you have one copy with a C, and one with a T.
And yea, it's normal for the first several thousand, or million letters to be N's.  The genome is repetitive and yucky there, but it's counted for numbering purposes anyway.
Honestly, I wouldn't do this with a giant text file of the genome.  Just search for your SNP in ensembl.org using the rs number, and you'll get the SNP, and some flanking sequence, and some context.  Search it in PubMed if you want to see if it's ever turned up in any publication

Part 1:
According to Lior Pachter, 23andme data are not phased. Which means that for each entry in the genotype field, you do not know which chromosome copy it came from. This happens since modern microarray platforms are not able to tell which of the two copies of a chromosome a snp came from.
You can solve this problem for most snps by comparing your alleles to the reference genome, but this would take some programming chops. You could use https://github.com/endrebak/qc_gwas as an example, which does the same thing, but for plink files.
Part 2:
I'm assuming that you would like to do this programatically, and not by copying and pasting the snps into the reference genome.
The short answer is that the first N is the first nucleotide. But, you should rather use a package such as Biopython to do the counting for you, it might be knottier than you think (you need to adjust for line endings in the fasta file, for example).


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Exercise vs stimulants, which is more effective for promoting concentration?
Stimulants are the first choice for treating ADHD. But we also know that exercise helps to improve concentration.
We know that both stimulants and exercise increase bloodflow to muscles and to the brain by activating the sympathetic nervous system. Is this is the MAIN cause of the effect of improved concentration, rather than, say, specific activation of parts of the brain responsible for learning or planning or something similar?
What I'm asking is, do drugs and exercise have different effects on the brain, what are the differences, and what are the consequences of these differences on concentration and learning? Which is more effective for promoting concentration and why?

exercise stimulates brain regions that are involved in memory function to release a chemical called brain-derived neurotrophic factor (BDNF) which is a protein that helps in the survival of neurons and promotes the growth of new neurons. BDNF rewires memory circuits so they work better.
Memory enhancers or smart drugs or Nootropics as they are called help in improving the efficiency of neurotransmitters and its associated receptors in cognitive function. Three systems that are stimulated by these drugs which I could find are:
1) Cholineric System
2) Glutamatergic System
3) Dopaminergic & Serotonergic Systems
You can read about about them here along with links to published articles on their effects. Details of different nootropic drugs are mentioned in this article along with their effects.
Of course naturally improving concentration would be the way to go considering the hazards of long term use of drugs. Some links to the side effects are this and this

Thanks but can you give a quantitative comparison for example, by how much does exercise improve working memory capacity compared to modafinil? By cholineric do you mean cholinergic? I'd vote you up if I could.

Cholinergic is the abbreviated term for acetylcholine which is in fact the primary component of the cholineric system so you can say that both of them are basically the same thing.. Sadly, as of now, I cant find a published paper on comparing smart drugs with exercise. I would suggest you read papers on how much exercise improves cognitive function like this one (http://dev.europepmc.org/abstract/MED/17414812/reload=2;jsessionid=KueHPX5d2GFw4mgwWuGZ.0), read a paper on how modafinil affects cognitive function (http://link.springer.com/article/10.1007/s00213-002-1250-8) and form a comparision.