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Understanding the strategy of Sanger DNA sequencing
The Sanger sequencing method creates large numbers of sequences of all possible lengths, ending with a specific nucleotide, by terminating with a tagged (fluorescent) nucleotide at the end.
But if you already have fluorescent nucleotides of a specific base, why not just do regular PCR  with them, create a huge number of full length copies of the original sequence, and then simply see the locations where the nucleotide fluoresces to determine all the locations of that base. Why do we need a large number of copies ending at each possible location, as with the Sanger method?

It is unclear whether you are asking a) how the Sanger method works, or b) why it is used (or why it was invented) when Next Gen methods are better. However my guess is that you are student who has encountered DNA sequencing methods without any historical or practical context, and has got bogged down in the preparation of the samples rather than the methods for actually determining the sequences. Read Wikipedia on Sanger and more modern Sequencing  methods. (The Sanger method predates PCR.)

why not just do regular PCR with them, create a huge number of full
length copies of the original sequence, and then simply see the
locations where the nucleotide fluoresces to determine all the
locations of that base. How? What instrument do you propose to use to see the sequence of fluorescent tags?

If you mark the full length strand of the DNA with the fluorescent labels, you will get a lot of signals from the same nucleotide without the possibility to discriminate where the actual nucleotide is located on the strand.
Sanger sequencing doesn't end with the preparation of the terminated and labelled DNA strands, the following step is crucial in discriminating where the labelled base actually is. After labelling, the sample is run through high resolution capillary gel electrophoresis to sort them by size. The smallest fragment comes out first, then the one with one base more and so on. The detector which then identifies which fragment is coming through is located at the end of the capillary.
This works like shown in the schematic image (from here):

If you would mark a complete strand, no dicrimination by size is possible (ideally, all DNA would run on the same height of a gel) and all flourescent signals for all positions would come on the same spot. Not very helpful.

Additionally, the original method of Sanger didn’t use labelled ddNTPs at all. The sequence was determined solely on the basis of fragment size and knowledge of which ddNTP terminated it.

And the Sanger method didn't use capilliary gel electrophoresis for many years after its inception. The principle is merely separation, which in a single small laboratory is proably still done by slab gel electrophoresis.

Foreword
I originally suggested closing this question as I think it confuses methodological details with strategy. There is an accepted answer that clarifies things with a clear diagram of the Sanger method. In the circumstances I decided to add a different sort of answer — one that emphasises the principles involved in the different approaches, rather than practical details which are not intimately associated with logic of the different approaches.
General Strategy of DNA sequencing
Irrespective of the method, the determination of DNA (or any linear) sequence requires two pieces of conceptual information:

Knowledge of a particular position in the sequence.
The identity of the base at that position.
This is illustrated in the graphic. In addition, there is a practical requirement:
Means to uniquely detect this.

Let us compare these in three different sequencing approaches.
A. Chemical fragmentation (Maxam & Gilbert)
Here the DNA to be sequenced labelled at one end is treated with different chemicals that cleave at different bases in separate reactions.

The position is indicated by the length of the fragment.
The base is known from the chemical used.
Detection is performed by separating the different fragments by length and using their radioactivity to visualize them (by autoradiography).

B. Chain termination during synthesis (Sanger)
This method uses enzyme-catalysed copying of  the DNA to be sequenced, with termination of the copying produced by the four di-deoxy analogues of the deoxynucleotide triphosphates (dNTPs) in separate reactions.

The position is indicated by the length of the fragment (as in A).
The base is known from the particular di-deoxy analogue used to terminate the reaction.
Detection is performed by separating the products of synthesis by length and using the radioactivity or fluorescence of the dNTPs used in synthesis to visualize them.

(Note to the poster: obviously you need fragments of all different lengths if you are going to identify the base at each the position in the chain.)
C. Phased synthesis (‘Next Generation Sequencing’)
This type of method also uses enzyme-catalysed copying of  the DNA to be sequenced. However, there is no termination of the chains, as in B, but the cycles of addition are followed by various techniques.

The position of a base in a sequence is indicated by the cycle of addition at which the insertion of the base is detected.
The base is known from which of the different dNTPs allow the extension reaction to occur.
Detection methods vary but include detecting the release of pyrophosphate by coupling to a light-emitting reaction (pyrosequencing) and detecting hydrogen ions released during the polymerization using a semiconductor chip (ion torrent).

Coda: Principle and Practice
In stressing the general principles of DNA sequencing the methodology mentioned has been limited to that required for detection — there was no need to even mention PCR. Of course, different methodologies for preparing multiple samples for sequencing have hugely influenced the speed and cost of DNA sequencing. However the student should understand the principles before getting bogged down in the details, which can be found e.g. in this Wikipedia article on sequencing and on the website of ATDBIO (albeit a not disinterested company).


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Glycosidation and glycosylation
I read somewhere that the function of Golgi bodies is glycosylation and glycosidation. What is the difference between the two? I searched google but it gives complex answers.

“I read somewhere” is not adequate for this list. Unless you can tell us where and either cite in full we cannot assess the accuracy or examine the context of your assertion.

Glycosylation is a controlled process that involves a carbohydrate being attached to a hydroxyl or other functional group of another molecule. I think you meant to say glycation instead of glycosylation, and that is a random process that involves free sugars attaching to proteins.
https://www.neb.com/faqs/2015/04/10/what-is-the-difference-between-glycosylation-and-glycation

Welcome to [biology.se]. Can you please add some references to support your answer? References are useful for users to verify the answer and for understanding the topic better.

Sure, my bad. https://www.neb.com/faqs/2015/04/10/what-is-the-difference-between-glycosylation-and-glycation

Thanks for the reference. Please [edit] your answer to include it. Comments are only meant for temporary suggestions/requesting clarifications.

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Nature versus nurture regarding aggression in specific dog breeds
A week ago I was bitten in my face by a dog that originally came from an asylum. That dog is half Rottweiler. Some people claim that the history of the dog is probably different from what the asylum thinks or says, whereas other people claim that Rottweilers or male Rottweilers are unreliable. But let's not focus on this single occurrence and ask the wider question:
Is there scientific evidence to indicate that there are certain breeds that produce significant numbers of dogs that are inherently and unreliably aggressive, or is such aggression usually the consequence of how their owners raised them?

How are dogs political? Anyway, we don't do political discussions here — they get vacuumed up very quickly.

@David An answer to the question would be an argument in the political debate whether certain dog breeds should be banned, as was once the case in Belgium.

I see. But, as I said, this SE is only for objective biology questions and objective answers. In general I would advise not anticipating trouble with your post — it is more likely to provoke it than otherwise. Trust in the good sense of members until they prove otherwise, and then flag any inappropriate responses to the moderators.

It seems that there are some important differences in dog aggression depending on the dog breed (towards strangers, owners, and other dogs):

That being said, it seems that a significant proportion of a dog's behavior can be due to its environment (training, etc), according to a study, this 'nurture' component might explain up to 80% in the variation in aggression (which should be considered when interpreting the other study I cite).

For discriminating viewers: the error bars indicate a 95% confidence interval, i.e. the range of values for which we can be 95% certain to contain the true mean of the population. Notice the error bars are quite wide. Notice also the scale bars; we are always talking about < 1% of dogs (1-3 out of 138 dogs on average) so I would be wary of these pretty tiny differences. We're talking about being hit by lightning vs. winning the lottery statistics here. Interpret them with a grain of salt!

For even more discriminating viewers: Notice the Y-scale represents a value that can vary in the [0,4] interval, which is the interval used in this particular technique (0-no aggression, 4-most aggression). So, these are not 'pretty tiny differences'. Basic statistics are easy to be misinterpreted. More info: https://sci-hub.tw/10.2460/javma.2003.223.1293

There are also very few other studies that replicate any dog breed findings. I would be as cautious as the authors themselves, who in their own words state that "the substantial within-breed variation in C-BARQ scores observed in this study suggests that it is inappropriate to make predictions about a given dog’s propensity for aggressive behavior based solely on its breed." And remember that the data is based on subjective questionnaire reporting online, which is difficult to gauge as trustworthy or true to reality, especially since we are talking about pets!

You're on your right to be cautious, but 259 other papers citing this study are not "very few": https://bit.ly/31WZtDH - in any scientific field (biology specially) that is quite a significant number of citations. I quote another study citing the paper: "questionnaire surveys provide more detailed information about the dog's behaviour than behavioural tests, especially about low-frequency behaviours (Duffy et al., 2008)". (https://bit.ly/2MmDqzO). I'm sure the study is not perfect, but criticizing its statistics/design without knowledge of the matter is not very scientific either.

There is another study, in addition to that cited by @TumbiSapichu, that establishes a genetic component in canine aggression. This is: Zapata et al. (2016) BMC Genomics 17:572 and is entitled Genetic mapping of canine fear and aggression.
The study did not set out to establish which breeds, if any, are most aggressive, but started from the proposition that there might be a genetic component in canine aggression, and tested this by a genome-wide association (GWA) study on one cohort of different breeds. This established certain candidate genes, which were tested — and confirmed — on a second cohort. The authors of the paper conclude:

“We have mapped many canine fear and aggression traits to single haplotypes at the GNAT3-CD36 and IGSF1 loci. CD36 is widely expressed, but areas of the amygdala and hypothalamus are among the brain regions with highest enrichment; and CD36-knockout mice are known to have significantly increased anxiety and aggression. Both of the other genes have very high tissue-specificity and are very abundantly expressed in brain regions that comprise the core anatomy of fear and aggression – the amygdala to hypothalamic-pituitary-adrenal (HPA) axis. We propose that reduced-fear variants at these loci may have been involved in the domestication process.”

I appreciate that the reader may wish to see a graphic showing that Rottweilers are more aggressive than Yorkies, for example. However the paper clearly answers in the positive the question of whether there is a genetic component in canine aggression, and the paper has 20 pages and eight figures for anyone who wishes to tease out information regarding specific breeds. (I do not own a dog, so lack the incentive to do so myself.)

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Is there any standard of notation for ecological diagrams?
General Question
Is there any convention of how to express different types of relations (e.g., eats, turns into, is beneficial to) and agents (e.g., species, nutrient) in an ecological diagram? I know that inhibitory relationships are indicated by barred arrows, but I failed to find anything going beyond this.
Example
Suppose, I want to express that Species A excretes Nutrient X, which in turn is metabolised by Species B. Naïvely, I would sketch this as follows:

However, this it not necessarily clear:

I here arbitrarily used squares and circles to distinguish species and nutrients.
If you do not know this, you could not immediately distinguish them.
(Of course, I may just use specific examples like tree instead of A, but then for my theoretical cases, a tree is too concrete.)
The arrows mean different things.
The left arrow means excretes, the right arrow means is metabolised by.
Moreover, the arrows could be mistaken for something like turns into or a general is beneficial to.

How would I denote the above relation unambiguously in a diagram?


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How much variation in mutation rate in there in the human genome?
In humans, the average mutation rate is estimated to be around $2.5 \cdot 10^{-8}$ (Nachman and Crowell, 2000). Of course this mutation varies from sequence to sequence.
Can you please give some ideas of how much variation in mutation rate there is in the human genome?
There are many ways to express such variation. One could give the lowest and highest mutation rate or shows a mutation rate map over either the whole genome or a randomly chosen sequence.

Cool question. Unfortunately, I don't have a complete answer; the best I can do is summarize some literature. I'd be happy to look more if you want to discuss though. Also, sorry the answer is a little scattered and I apologize if you were already aware of all this!
One thing I will suggest though is that this is hard to do for the human genome in isolation; hence why much of the literature draws on other animals as well.
In any case, the literature on this topic is quite expansive, so I am afraid this is merely the tip of the iceberg. Hopefully it's helpful though.

Firstly, I know of two genomic mutation rate maps that might interest you (as you suggest in your question). One in Genome-wide patterns and properties of de novo mutations in humans by Francioli et al, looking at de novo mutations in humans (obviously more concerned with germline mutations), and another in Mutational heterogeneity in cancer and the search for new cancer genes by Lawrence et al, which (unsurprisingly) is concerned with somatic mutation rates and the resulting oncogenics.
A great review, although not entirely human-specific, is Variation in the mutation rate across mammalian genomes by Hodgkinson and Eyre-Walker. They note that:

Small-scale effects: G & C mutate more than A & T, CG dinucleotides are highly correlated to higher mutation in non-coding DNA, and there appear to be hyper-mutable sites (conserved across species) that are susceptible to SNPs. These effects vary across the genome as well. Indeed, certain regions of mitochondrial DNA also have highly variable mutation rates. Oddly, GC-rich islands may be less mutable (for certain mutation types), and may affect nearby nucleotides, particularly methylated ones.
Transciption sites: somatic tissue has lower mutation rates of transcribed areas than non-transcribed ones. In germ tissue, there is an interesting effect for certain types of mutations increasing as one moves away from the transcription start site, but not others.
Other mutations: indel mutations tend to co-occur with point mutations
Mutation rates are spatially correlated at multiple scales.
Chromosomes: for humans, it seems the Y chromosome is the most mutable, followed by the X, and then the autosomes. There is also a difference in the mutation rate between autosomes, but it appears this is overshadowed by the intra-autosomal mutation rates.

Not explicitly noted by the paper, but intutive and sometimes implied, is the lower mutation rate in coding and regulatory regions (e.g. enhancers, promoters,...).
Another paper is Evolution of Local Mutation Rate and Its Determinants by Terekhanova et al. They note local mutation rates in primates (obviously including humans) are highly correlated across the genome. This correlation weakens as evolutionary distance grows (e.g. humans to mice). They also look at the influence of several genomic features on local mutation rates.
Not in humans, but Evidence of non-random mutation rates suggests an evolutionary risk management strategy by Martincorena et al look at mutation rates across E. Coli genomes, finding enormous variability, particularly lower rates in highly expressed genes.
Since we have not yet seen chromatin structure pop up much, I'd like to point out the cool paper The effects of chromatin organization on variation in mutation rates in the genome by Makova and Hardison. Therein, they find that mutations of different types are affected differently by open vs closed chromatin states; roughly, closed chromatin encourages base substitutions, whereas indels occur more often in areas with open chromatin.
Finally, some of the difficulties in assessing mutation variability are explained by Eyre-Walker and Eyre-Walker, in How Much of the Variation in the Mutation Rate Along the Human Genome Can Be Explained?

Some related work
For mutation rates in germ-line cells specifically, see:

Properties and rates of germline mutations in humans by Campbell and Eichler
Determinants of Mutation Rate Variation in the Human Germline by Segurel et al
Variation in genome-wide mutation rates within and between
human families by Conrad et al

which describe some patterns in mutation variability across the genome, but are often more concerned with inter-individual factors.
Also here are two early papers using comparative genomics to look at mutation rates:

Mutation rates in mammalian genomes by Kumar and Subramanian
Deterministic Mutation Rate Variation in the
Human Genome by Smith et al

which focus on inter-species comparison, but also discuss compositional differences (e.g. GC richness).

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Found a larva in my broccoli, is it a Small White (Pieris rapae)?
Found this living larva in broccoli from a store. It was about 10 mm long. It was in july this year, and I don't remember the country of origin for the broccoli. A bit of googling makes me think it could be a Pieris rapae, but I don't know if there are any similar species.

edit: Even if I don't know the origin of the broccoli, I assume (and hope) it was grown in Europe since I got it in Sweden.

It definately looks like a Pieris rapae larvae, which are distinct from larvae in closely related common species as e.g. Pieris napi and Pieris brassicae. However, I'm not a lepidopterist and there might be related rarer species I'm not aware of, especially since you don't know where the broccoli is from. However, Pieris rapae is found basically all over the world as native or introduced (native in Europe, Asia, Africa and introduced in e.g. Ameria and Australia) and is a pest species of cabbage (including broccoli) so it is a very good fit.

Tried asking in another forum, and no one had an alternative to Pieris rapae, so I'll go with that until a lepidopterist objects!

@picapica Based on your update; if found and probably grown in Sweden, it if definitely Pieris rapae. Nice gifs on your tumblr by the way. The spider-killed syrphid fly here from 18th Aug. is a Volucella pellucida (Fönsterblomfluga), and the beetle below is probably Phyllopertha horticola.

Thanks for the bonus taxonomy, much appreciated. (I don't really dare to use this place to ask about all the animals that I wonder about, that would most likely become spammy...)

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Constantly wiggling moth pupa - will it emerge soon?
Today I found a moth pupa in the soil in my garden in western Sweden. It's about 15 mm long.
I have found similar ones before, but this one is wiggling a lot more, even after I put it down and put a bit of dirt over it. It's been moving for more than an hour now, but less now than in the beginning.

I was hoping to see it emerge, but if it will take more than a day or so, I will probably put it back. So, what I'm wondering is if this wiggling is any indication of how soon it will emerge. Or if there are other ways to tell.
Update: an hour later it has stopped moving. Maybe it was just very disturbed by my presence. I'm keeping it in a jar with soil and a stick for climbing up on, and I'll decide what to do with it tomorrow.
Update: 12 hours later and it seems very still. But I'm letting the question remain since I really want to know if there are any signs to look for.
Final update: After 16 days it had turned almost black, and was still very active when handled.

And after 17 days this moth came out:

I posted the same question on tumblr and got an answer:

It depends on the species. This one looks like a Noctuid. I’d give it
  two weeks to a month or so. You may be able to see its wings showing
  through the darkening pupal case when the time draws near! Just make
  sure you give it somewhere to climb up and expand its wings when it
  ecloses.

After keeping it until the moth emerged, I now know that wiggliness is not an indication of maturity, but turning dark is.


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Is it possible to increase lifespan through controlled evolution?
A few years back when I was reading The Selfish Gene by Richard Dawkins, there's this short passage where he theorizes about a way to achieve an increased lifespan through controlled evolution.
The theory goes like this: we don't tend to have medical problems until after 30 because we all tend to reproduce before that age.  Thus, people who tended to die before 30 never passed on their dying-prone genes.
So, if you didn't let people reproduce before a age X (where X starts at 30) and then slowly move that age up, you could use evolution to increase lifespan.
The ethical issues notwithstanding, is there any reason why this wouldn't work?  If it would work, how long do you think you would need to sit at each value of X?  How far apart do you think each value could be?  Finally, how many generations, using this technique, would it take before someone would live to be 1000 naturally?

The well quantifiable subject of say e.coli evolution is a totally different matter than say human evolution on aging, no less. This subject in the way it is phrased may be better suited for skeptics.SE (which is meant to discuss the information provided by notable sources).

@LoSauer I see no great difference between E. coli and human evolution. They same forces drive both of them. Granted the human genome is orders of magnitude more complex than that of E. coli but nevertheless, the governing principles of evolution are the same in both cases.

@terdon bacteria have a lot more lateral gene transfer and can acquire plasmids to add new chromosomal material.  They also have co-regulation through operons.  Prokaryotic and eukaryotic selection and evolution are remarkably different, at least to the level of mechanisms described in this question.

All true @shigeta, I am just saying that the driving force of selection still depends on the time that an individual reproduces, whatever way it does so, be it sexual or budding or whatever. In any case, this is a discussion I would love to have over a beer some time but not really appropriate for the comments of the poor OP's question. Unfortunately. Maybe we can continue it in chat at some point?

@terdon wish we could get a beer.  not only would the conversation be welcome, but that could mean I was in France!  Its been a while :)

before that age -> after that age, perhaps?

I think this would probably work.  The grandmother effect, which is one of the main theories for human longevity after fertility might indicate that human lifespan would increase if the children come later.
Just have to disclaim here: We will never do this.  Many unthinkable consequences would result...
If you simply forbid anyone to have children before they are 40 or 45 (fertility doesn't drop until age 35 or so), forbid invitro fertilization and medical assistance to conception we would probably be looking at a prolonged lifespan.  Infertility rates in women at age 40 are not clear, but one estimate is that 40% of women can have children at 40 years of age.  If we want to seen an effect early, we would push the age up a year or two.  Forbidding in vitro fertilization and other medical assistance to offspring we could look like a 80-90% cut of people - lots of people would never have children.  This might make people unhappy an destabilize the social fabric.
Its not clear how long this would take.  The generation time would go to 40 years from about 20 now - 40 to get to childbearing age, but results would take 80 years - when we find out how the children would fare.  Given the C elegans longevity experiments and the fact that we are starting with 8 billion people, we probably would find some great late age breeders who may also live long.  But for the longevity phenotype to set in it would take several generations as we are looking for an indirect effect: later breeding causing longevity.  The Belyaev experiments which produced domesticated foxes by strong selective breeding took some 30ish generations to complete though they saw a significant effect in just 10.  It could take a similar numbers of selection rounds in this cse.  4-500 years. Ethical issues aside, this is why most geneticists study flies.
There would also be a lot of other negative socioeconomic consequences to this thought experiment.  One good thing is that the population of the earth would plummet - many people would be eliminated from the gene pool, though eldercare would be a major part of the world workforce.  Lots of work, not clear who is going to pay for it, but low unemployment and low low wages may result.

So you see Mister President, this is quite a distinct possibility, though some sacrifices would have to be made.
The science of human eugenics is not scientifically wrong, but selective animal breeding and lab experiments don't usually evaluate or care about the consequences of large peturbations in the gene pool.
You would also have a lot more autism and Downs syndrome and other congenital defects which tend to show up in offspring of older parents. These issues might improve with application of biotechnology which screens weak sperm and eggs without ruining the effect you are looking for, maybe not.
Since we are selecting against fecundity, the human race could be dogged by fertility problems or chronic genetic diseases which the genetic contribution of some of the more robust people in the gene pool being removed and the tendency to such age-related birth defects might not go away given the drastic selection pressure we are putting on the gene pool.
Other consequences you might not expect; some physical traits associated with longevity and prolonged fertility would cause us to look more alike and not necessarily in a good way.   Browse the internet; its probable that we would get shorter and possibly uglier?
There are many more direct ways to increase the human lifespan - better diet, exercise, the elimination of poverty, vaccinations, proper medical care, access to clean drinking water and a lower birth rate (fewer children not later) all are known to directly effect longevity, having more than doubled the human life expectancy in the past few hundred years.

What a great answer. +1

A potential side effect of the selection would be a substantial delay of the age of puberty, as to, say, 30, which would effectively extend childhood.  Longer lives are usually correlated with later age of sexual maturation.

@mgkrebbs yup this is one possible part of an outcome.  All of this can be imagined when one looks at what happens to domesticated foxes - they became more juvenille in appearance when they were genetically tame.  would all people also start to look older when they are younger?  not sure, but stimulating to think about.

This has been done in fruit flies. At least two labs have used selection to breed longer-lived  flies.
Rose, M. Laboratory Evolution of Postponed Senescence in Drosophila melanogaster. Evolution (1984).
Luckinbill, L. et al. Selection for Delayed Senescence in Drosophila melanogaster. Evolution (1984).
We won't do this to humans, because eugenics is evil.
The "methuselah flies", as Rose calls them, live about twice as long. I don't know how long it would take to get them to live 10 times as long. In any breeding program you run up against the problem that eventually you'll run out of standing genetic variation to select from, and you have to wait for new mutations to appear.
But obviously selection can eventually lead to the evolution of much longer life. This has happened many times in evolutionary history, for example.

Eugenics is just a method, why would it be inherently "evil"?


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How many people are required to maintain genetic diversity?
Imagine humans were to colonize a distant planet and it was a single one-way trip. How many people would they need to bring?
Obviously 2 is the minimum, but that would result in a lot of inbreeding.
So what number is the minimum number of people you can have in an isolated community and still maintain a healthy diversity?

Without doing any digging, my understanding is that first cousins can really interbreed without too much risk.  So a first estimate that 2 completely unrelated mating pairs from distant parts of the human genetic tree might make a minimal  gene pool candidate.  I can see an argument being made for 8 too.

It depends on how you select the people, if they are carefully selected for genetic diversity you might be able to get away with a hundred, but  you have problems if even a few people die, which is not unlikely in a completely new environment. So even with careful selection and breeding controls you still want a few hundred. the more other things like skills matter the more people you need becasue you can't just select for genetics which brings you closer to 500 individuals. If people are selected more or less at random (genetically) you want more than  a thousand.

The big problem is NO  new genetic material is going to be introduced (aside from mutation), and the population is going to be expanding, dying, and need to continue into perpetuity.  So you need a a lot of initial diversity. This isn't a  lab study where you only need to maintain for a few generations.

Actually it is a very important question for laboratory animals (and, I imagine, endangered species) and was calculated to be 25 couples.
With any number of animals (including humans), there is always some inbreeding happening, but you can reduce it with the number of breeding pairs and careful pairing. When you get to 25 pairs (50 animals) and have complete control over pairing, you can sustain the genetic diversity practically infinitely (especially if you take into account spontaneous mutations).
Of course, such control over who can have children with who (plus whether one is at all allowed to procreate and what will be the sex of their children!) would be questionable morally, so in case of populating a distant planet, we would need a larger group, to provide for sexual preferences, fertility problems etc.
Some information on laboratory outbred stocks.

nice answer - it makes me realize though that there are problems keeping some dog breeds viable - they tend to accumulate too many diseases (link below).  Yet there must be thousands of animals in most breeds that are in trouble.  Is this because controlled breeding is used differently (emphasizing breeding traits vs diversity), because there was few original dogs in the pool, or why?  http://www.nytimes.com/2011/11/27/magazine/can-the-bulldog-be-saved.html?pagewanted=all&_r=0

I am no expert on dogs, but did learn a bit about in- and outreeding. Each dog breed is either open or closed. In a closed breed, only offspring of animals already belonging to this race belong to the race. In an open breed any animal that looks similar enough (or has other important traits, characteristic for the breed) can be a parent of a "breed" litter. Under certain circumstances (e.g. too few animals in the breed, too bad overall health of the breed) a closed breed can be opened and after the problem is solved, closed again.

How did people arrive at this number? The linked article doesn't seem to explain it.

It's just mathematics. If you pick two outbred mice/rats etc. and mate them, the offspring is about 0,5-1% more inbred than their parents (meaning both their copies of any gene are a tiny bit more likely to be inherited from one ancestor mouse). If you have enough animals, this effect is smaller than the effect of other phenomena, such as genetic drift (compare with the assumptions behind Hardy-Weinberg equilibrium). I don't know the exact equasions behind those numbers, I just know, that this was calculated and such-and-such numbers are used.

I don't think it's that bad to control who has children with who. It's not like you're controlling who is in love with who or who is having sex with who. You're just making sure people use protection and get inseminated with the proper sperm when they're ready for children.

Have you considered women's point of view? That in this scenario somebody decides to use a woman's body to generate some number of children and you cannot decline, you are literally forced into pregnancy? Pregnancy and childbirth, which, even with modern medical advancements, are an important cause of death for women?
I guess the people who board such a ship can make this kind of a decision, but their children would not be given any choice with regard to bearing a second generation.

The sentence When you get to 25 pairs [..], you can sustain the genetic diversity practically infinitely is wrong IMO. At equilibrium, genetic diversity is a simple function of the effective population size. There is no minimum size to sustain the genetic diversity practically infinitely. There is some genetic diversity with only 2 people and there is more genetic diversity with 50 people and even more with 100k people and the is no such as THE genetic diversity

I'm not an expert, but after reading more about it I would say between 500 - 1500 couples without trying to control the pairing.
I don't know where Dan Horvat took these assertion:

To maintain healthy genetic diversity and establish enough different
alleles to allow for sustainability of the species. I don't remember
the exact number but I think for humans it was something between 1000
or 10000, and if you get below that number the species will likely go
extinct by natural causes.

but it seems to be supported by the evidence of past bottlenecks in human population, like the Toba Cathastrofe Theory. The human population is supposed to had a maximum of 3,000–10,000 surviving individuals. I am very optimistic and take the minimum: 1500 couples. It left to match that amount with Dan's source.
The exact answer would come by the designer of the life and DNA. ;-) That info seems to have been leaked by the creator's son in a conference. Thomas has taken note from his words:

I shall choose you, one out of a thousand, and two out of ten
thousand, and they shall stand as a single one.

It seems to me that it is talking about genetic diversity, and the minimal proportions are those: 1/1000. That's why I take 500 couples as minimun.
By the way, in the previuos versicle it seems to says that that selection would be in the moment when the human race has finally ended evolving to the intended social and morphological status (very rare indeed):

When you make the two one, and when you make the inside like the
outside and the outside like the inside, and the above like the below,
and when you make the male and the female one and the same, so that
the male not be male nor the female female; and when you fashion eyes
in the place of an eye, and a hand in place of a hand, and a foot in
place of a foot, and a likeness in place of a likeness; then will you
enter the kingdom.

Going back to science, it seems that not to much effort should be made to control the pairing, because we seem to have a subconcient attraction for those individuals of the other sex that present better histocompatibility with us. In the case of humans given by odor and appeareance (mostly simetry).
Also the genetic diversity is supposed to be reached faster, if the environment is more aggresive. Normally a big mutation and adaptation happen after hostile and persistent environment over near 40 generations, something observed with the Peppered moth evolution
So I suppose that if you use well cared laboratory animals, the number can be 25 couples. But if you use a natural hostile enviroment the genetic diversity could be reached sooner.
It might be that if you build a nice human space station in another planet, maybe you need 25 couples, but if you let them nude with no technology and fig leaves you need fewer couples in order the species to survive more adapted (Although you might got many failed attempts)
Another point to consider, is how valuable are those animals for genetic studies?, how much is the study affected by the captivy of their population?, resembles their growing places the natural environment?, how hostile are these environment? resembles this environment the natural population dynamics ? how many generations ago their ancestors had a natural environment ?
Laboratory animals might have less genetic diversity and might need more couples.

The distinction between this being the correct answer and the one chosen, has to do with the level of genetic preselection. I agree that a minimum of 1000 "randomly chosen" people would be required, as one must not forget the impacts of homosexuality and varying levels of "fidelity" in mating pairs.

I guess than homosexuality and fidelity might have also to do with epigenetics and the needed dynamics of the population.
In some fishes like: "Lythrypnus dalli" , even the genre of the individuals changes at a morphological level according to the necessities of the population. (https://www.sciencedirect.com/science/article/pii/S002209810400680X)

Also it might be that less individuals and good conditions  for expanding the population generates less "fidelity".

At the contrary, an excess of genetic diversity in a population (if such concept exists) might generate more fidelity.

I think the issue of epigenetics throws this answer into debate once again. This reminds me of my biggest issue with the book The Transhumanist Wager, which was centered around a very Libertarian tenant of "worth".
Without knowledge of the way in which every aspect of human genetics (including epigenetics) works, how can we possibly establish the "worth" of a given set of base allele, and thus determine minimum viable population? If such a bottleneck were forced (through disaster or "choice") would such a resultant population still be considered "human" by today's standards?
I would say that Humanity must still be defined by more than the sum of our current knowledge of genetics.
I believe these questions are something that are very often missing from the debate around The Singularity [establishing an artificial intelligence beyond the intelligence of humanity]. Most argue that such an event would be the end of humanity, but I disagree; as any intelligence created by humanity would not be so stupid as to destroy the diversity of intelligence that essentially established its baseline. In this line of thinking, personally I believe it would be more along the lines of the ideas presented in the movie Her, in which such Intelligence(s) would establish a way to remove themselves from direct human control, but ultimately observe/compare/contrast humanity as "wild stock" useful for error-correction, and a seperate line of modeling.

Inbreeding isn't negative at all, so one couple would suffice for colonization.
Inbreeding fixes recessive traits and the ones displaying unwanted traits can be culled. Actually, inbreeding is one of the most potent weapons of evolution, it speeds things up greatly. We went through a major bottleneck event ourselves and lived to tell the tale.
The exact number of individuals needed for a healthy species that will survive X number of generations depends on the species though. To maintain healthy genetic diversity and establish enough different alleles to allow for sustainability of the species. I don't remember the exact number but I think for humans it was something between 1000 or 10000, and if you get below that number the species will likely go extinct by natural causes.
Of course, everything is completely different when you have full control over who mates with who. But still, in the above example of 1 couple, they can successfully start a seemingly healthy population, but due to low genetic diversity they - as a species - won't be able to respond to, say, increased radiation, changes in atmosphere, a virus, bacteria, shortage of food, etc. That's why 1 couple is basically enough, but to ensure longetivity of the species 25 couples is far from enough.

And if the undesirable trait is recessive, how do you cull it?  Queen Victoria had the allele for hemophila, and after a few generations, it was in all the European royal houses, with multiple people suffering from the disease.

You cull a trait by simply not procreating the specimens who have that trait. But, first of all, some genetic diseases are not noticeable before old age so you can't know about them unless you study the genome, and second of all it isn't ethical (or desirable, but that's a different story) to cull humans. Especially if it's the Queen. In case of haemophilia, a female can be the carrier but rarely has the disease. It just shows up with certain males down the blood line and in that day and age they didn't know why.

Actually, that's a much more complicated case. The short answer is: you can't be completely certain you've culled the recessive allele. You can diminish it's frequency and this has been done in a neat way in the Mediterranean with thalassaemias (a group of diseases related to sickle cell anemia) - young couples with non-negligible risk were tested and if both carried the gene, they were advised against having children or given access to abortion if the fetus turned to be sick. Given stricter control, reduction could be achieved fasted, but when the allele becomes rare, it gets more difficult.

Dan Horvat's scenario is only theoretically feasible. People have, on average, 15 damaged genes that may lead to a deadly disease. The first couple (and next generations, too) would have to produce lots of children in order to give them a good chance of findinf couples who can have healthy children. Much more likely this scenario would result in a population with uncommon genetic diseases being common, like in Finland (which artificially created a series of bottlenecks from the 17th century, a fascinating story), read more here: http://www.cs.sjsu.edu/~khuri/Aalto_2010/Norio_2003.pdf

Hey, Dan. Where did you got these numbers from: "1000 or 10000" ?

The reason similarity is bad is the more genetically similar the population the more likely a single disease will wipe them out. That is before you get to things like recessive traits.

You only need a single female. The space ship could carry a database of genetic material in the form of frozen sperm and eggs. The first female would impregnate herself to breed and raise as many daughters as she can, using as much genetic variety as possible. The daughters would do the same once they can.

Welcome to Biology.se. You should always add references for your claims.

I didn't mean to convey the scientific insight that the OP was presumable looking for; I was hoping that would be clear. This answer points out a logically valid alternative interpretation of the question.

In this case yours is probably more suitable as a comment


text:
The probability of indirect human fertilization?
What is the probability of conception in situations when sperm isn't directly ejaculated into the woman's vagina, like:

The man's or the woman's hands come into contact with sperm, for example when removing a condom. (Perhaps after washing them,) the hands later touch vagina, for example during foreplay to another intercourse.
The man and the woman taking a bath together, the man ejaculates into the water.
The man ejaculates on the woman's body, perhaps on or around vagina but not inside. (In this case it could also make a difference whether the woman has shaved pubic hair or not.)
The man ejaculates during receiving oral sex, (perhaps the woman rinses her mouth), the couple kisses, the man performs oral sex to the woman.

In all these situations, it seems possible that a tiny amount of sperm is eventually transferred into vagina indirectly. And since just a single cell is enough to fertilize, it seems that there is non-zero probability of conceiving.
How much care need to be taken to prevent conception in such situations? Does simply washing sperm away with water (+ soap perhaps) eliminate it?
If you think of similar situations that are similar, please don't hesitate to add them.

Some outlandish claims of pregnancy: http://www.liveleak.com/view?i=e79_1351515813   and    http://www.museumofhoaxes.com/hoax/archive/permalink/the_case_of_the_miraculous_bullet    and    http://www.newspitter.com/2012/01/09/woman-gets-pregnant-after-having-intercourse-with-dead-man-in-a-mortuary

I don't have answers to all of your questions, but here is one example of a highly unusual conception via the gastrointestinal tract: http://blogs.discovermagazine.com/discoblog/2010/02/01/ncbi-rofl-thats-one-miraculous-conception/.
To cut a long story short, a woman born with a congenital defect that caused her to have no vagina was stabbed in the abdomen when her boyfriend found her performing fellatio on another man. She was taken to the hospital and patched up but a few months later:

Precisely 278 days later the patient was admitted again to hospital with acute, intermittent abdominal pain. Abdominal examination revealed a term pregnancy with a cephalic fetal presentation. The uterus was contracting regularly and the fetal heart was heard. Inspection of the vulva showed no vagina, only a shallow skin dimple was present below the external urethral meatus and between the labia minora. An emergency lower segment caesarean section was performed under spinal anaesthesia and a live male infant weighing 2800 g was born…

The article concludes that:

A plausible explanation for this pregnancy is that spermatozoa gained access to the reproductive organs via the injured gastrointestinal tract. It is known that spermatozoa do not survive long in an environment with a low pH (Jeffcoate1975), but it is also known that saliva has a high pH and that a starved person does not produce acid under normal circumstances (Bernards & Bouman 1976). It is likely that the patient became pregnant with her first or nearly first ovulation otherwise one would expect that inspissated blood in the uterus and salpinges would have made fertilization difficult. The fact that the son resembled the father excludes an even more miraculous conception.”

wow. That's all I can say...

Strictly speaking of course, this is not an answer to the question but still, +1 :).

Very very very very small. Next to impossible, millions of sperm cells start the journey and only a very small fraction of the sperm produced make it as far as the egg if "inserted properly." The vagina is a very hostile environment - to prevent infection - and this means very few sperm make it far enough. We produce in the order of 200-300 million sperm and it estimated that less than 1000 make it, so that is a 0.000005 chance of each sperm cell making it far enough.
There is also a benefit to travelling in such large number (each sperm is less likely to be destroyed by dilution effects, one sperm cell vs the entire human reproductive tract stands no chance). The numbers I am giving may be a little out from the correct ones, it's a while since I did my undergraduate module in sperm biology... I'm sure more accurate numbers will be  in this recommended reading
Further to this remember that not every attempt at fertilisation is successful even when doing it the right way, couples often try multiple times. If it takes 100 attempts to fertilise the egg just once the that is 1 in (100*200,000,000) sperm being successful.
Basically, if someone says they got pregnant sitting on a toilet seat that must have had sperm on it, or some other ridiculous claim, then simply don't believe them.

The man ejaculates on the woman's body

This won't lead to fertilization, as explained in the other answers, however, often times it happens after unprotected sex, meaning the penis was inside the vagina without a condom.
During intercourse, there is the pre-ejaculation fluid, that might arrive long before the actual ejaculation, and as answered here and here, it might contain sperm. The chances might not be very high, but it is possible.
To sum this up: while there is no indirect fertilization, some of the processes described in the question might mean that actions that took part before did lead to fertilization.


text:
Multiple sequence alignment - how to align everything to 1 gene sequence?
I'm having trouble aligning 3 sequences together - the total gene (~2500bp) and the forward and reverse sequences that are ~1000bp in length. Now I'm using Clustal X2, but the problem is that the program does complete alignment, which is useless for me right now.  Could anyone recommend or suggest any parameters or methods on how to align more that 2 sequences together, but that each sequence is aligned to the first one (the total gene)?
Thanks!

Which kind of result do you want to have? One alignment with three sequences, or two pair-wise alignments? If the former, what would you do if one of the 1000bp sequences causes a gap in the reference sequence?

Could you please clarify your question? The reverse strand of a sequence is not alignable to the forward strand. Also, i don't understand what you mean by complete gene, forward and reverse sequences. Do you mean the genomic sequence, the transcribed transcript and the reverse complement of that transcript?

Like the others, not sure that I understand, but if these 1000 bp sequences are perfect matches to the 2500 bp sequence then can't you generate what you want just by editing a file which shows the dsDNA sequence? Shouldn't take too long.

Multiple sequence alignment is a common bioinformatics problem and there are many tools available to solve it.
This paper provides a good comparison of the following tools:

Thompson, et al.  A comprehensive benchmark study of multiple
  sequence alignment methods: a current challenge and future
  perspectives

The paper addresses the following methods:

ClustalW
MUSCLE
DIALIGN-TX
KALIGN
ProbCons
MAFFT

this answer may be a bit sparse, but these are the most typical solutions to the question

If you want to align sequencing results over the reference sequence and check the sequences for presence of spontaneous mutations, the easiest way would be to use Sequlator.
Sequlator is a convenient because it has a pairwise alignment, reverse complement, editing and navigation functions but lacks irrelevant functions. With Sequlator one can manipulate any way existing alignments, or manually assemble sequencing reads into an alignment with the reference sequence. After elimination of poorly sequenced fragments, discrepancies with the reference sequence are revealed in the consensus of the resulting alignment. And it is free and Java-based meaning that it works on Windows, Linux and Mac computers

In Mafft, the command to align new sequences to an existing reference alignment is:
mafft --add new_sequences.fta existing_alignment.fta > output.fta

See this part of the documentation for more details.
It is a nice program to use for alignment, in any case...


text:
How to get smallest subtree containing a set of nodes from BioPhylo?
I'm testing out various phylogenetic libraries in Python. I want to read in a Newick tree, then, given a list of taxa, generate the smallest tree that contains them all. This task is quite simple and efficient in dendropy and ete2:
newick = '((raccoon, bear),((sea_lion,seal),((monkey,cat), weasel)),dog);'
taxa = ['raccoon', 'sea_lion']

import ete2
tree = ete2.Tree(newick)
pruned = tree.prune(taxa)

import dendropy
tree = dendropy.Tree.get_from_string(newick, 'newick')
pruned = tree.prune_taxa_with_labels(taxa)

I'm trying but failing to find equivalent functionality in the Bio.Phylo package. Trees do have a "prune" method, but it prunes a single node from the tree.

The common_ancestor function should give you the result you want: it gives you the tree (I think) that is the most recent common ancestor of all the given targets.

Sorry for digging out this old question. But I think that given you have an unrooted tree, the common ancestor maybe not the correct answer.
What you need to do is this:
Suppose you have an unrooted tree with n tips (species), and thus 2n-3 branches. You should cut the tree in half in all these possible branches. By doing this, you will have 4n-6 subtrees. The smallest subtree containing all your selected species will be your answer.
This is different from common ancestor because for an unrooted tree, it could be put in a way that those species not picked by you are clustered first, all your selected species becomes the outgroup. But if you "re-root" the tree properly, you could still make your selected species cluster together as a small, exclusive clade.

You are right that this wouldn't be correct for unrooted trees, so thanks for responding. I failed to mention in the question that the trees I was working with were in fact rooted (so the example tree was perhaps a bit misleading.)


text:
Distinguishing Father from Brother
Given the (non-identical) DNA sequences of two men and the knowledge that the second man is either the father, brother, or son of the first man, is the DNA useful in determining which of these three he is?  Even the slightest probabilistic indicator would be useful.

I will clarify your question a little. We start with two men, Dave and John. We know Dave and John are related, either as brothers, or parent-child. Can we use genetics to work out their relationship?
If Dave and John are brothers they will have the same mtDNA, the DNA in the mitochondria, because mitochondria are maternally inherited. They should have the same Y chromosome, because they have the same father (the Y comes from the father, and males have one Y to pass on, therefore they each received the same Y).
If Dave (John) is John's (Dave's) father, then they should have different mtDNA because they have different mothers (assuming that Dave (John) didn't have a child with his mother or sister, and that mtDNA is variable within the population). They would have the same Y chromosome, because that is paternally inherited.
If Dave and John have the same X chromosome it would be indicative of the same mother (there is a 50% probability that two male siblings will have the same X chromosome, while the probability of a father and son having the same X chromosome would be determined by variability of the X chromosomes within the population).
For the autosomal part of the genome, each parent carries two copies of each gene. This means that, in each gene, there is the potential for four different alleles, with two of those being passed to the offspring. For example, at gene $A$ the mother may have alleles $A_1$ and $A_2$, while the father has $A_3$ and $A_4$. The offspring receives one copy from each parent, with equal probability. The probability that a son receives $A_3$ from the father is 50%. The probability that a second son receives the same $A_3$ allele is 50%. Therefore, both father-son and brother-brother relationships have a coefficient of relationship of 0.5.
In summary, the mtDNA will liekly be the best indicator, but it is only indicative, it is possible (but highly unlikely in most modern societies) for father and son to share the same mtDNA.

You could, in principle, work out whether Dave is John's son or his father. For example (a really over simplified example), look at the diagram below. You first look at Dave's sequence and one chromosome in a pair has the sequence AAAAAAAAAA (Red chromosome) while the other has GGGGGGGGGG (Yellow chromosome). You then look at John's sequence and find one chromosome with the sequence TTTTTTTTTT (Green chromosome) and one with the sequence AAAAGGGGGG (Red & Yellow Chromosome). John could have received the AAAAGGGGGG chromosome from Dave after Dave's red and yellow chromosome recombined, while it is not possible that John is the father of Dave. John's green chromosome came from his mother.

+1 I am not quite aware about this but does Y-chromosome have enough polymorphic loci to differentiate close relatives? Is the variation in Y sufficient for these tests?

Depends really - a lot of the problems are methodological (sequencing the Y is difficult because of heterochromatin and repeat sequences) - and populations should be highly depleted for variation within, it would depend on the specific population and some regions of the Y generate new variation quickly (again, repeat sequences)... The key to the question is really the mtDNA, that's going to be the best indicator. The Y should be the same in both males regardless of the relationship.

@WYSIWYG I made some edits to clarify the points.

Also, perhaps you can add a note on how to differentiate whether an individual, X, is a son or a father of the other individual, Y.

@WYSIWYG I haven't considered whether this actually possible before, here is something that I think should work in theory

Another possibility is to look at imprinted loci.

I think you meant "there is a 100% probability that two male siblings will have the same X chromosome" and that Steve is John, right?

It's 50% - the mother has two X chromosomes, each will receive one of those with 50% probably that they get the same one. Well spotted on the name.

OK, I get it now and see why the mtDNA is the better indicator.  By the way, for bonus points, if I had changed brother to "half-brother from the same father" in my original question, is there a method?

Male half sibs would have the same Y and different mtDNA and X chromosomes - and they'd be related at the autosomal loci with a coefficient of relatedness of 0.25 (differing at the maternally inherited genes inline with population variance, at the paternally inherited genes having 50% probability of identity by descent)


text:
How much charge is moved for one heart beat?
Roughly, how much charge cycles (in and out of our heart cells) for each heart beat?
I am just looking for the total number of Coulombs, but, since all charge can
apparently be
accounted for with just $Na^+$, $K^+$, $Cl^-$, and $Ca^{2+}$ itemization,
it would be great if you can break it down by these ions.
My crude estimation comes from some $1\mu F/cm^2$ neuron wall capacitance
references, my guessed $10cm^2$ wall area (though the heart is bigger, I just
want the neurons), and the often-quoted $70mV$ action potential.  This gives $0.7\mu C$
(which is 4 trillion singly-charged ions).  But, I suspect that the true value
is much higher based on some other animal neuron papers that I found.

Most of the heart's electrical activity is in muscles, not neurons.

@BryanKrause I might have used the term "neuron" too loosely.  I am actually interested in all of the heart's electrical activity which factors into ECG waveforms.  So, feel free to change "neuron" to "muscle" in my question (unless the electrical activity you mention somehow gets muted in ECG data...and then it would of course be nice to explain the cause for this muting in any answer).

That's going to be quite the venture... the physics are incredibly complex, because while you generate voltages across membranes, these voltages are aligned in all sorts of directions and the vast majority cancel each other out when measured at a distance. Why do you need or want to know this? The reason you can measure an EKG at distance is because of spatial organization in the depolarizaton/repolarization of the heart: the top goes first. Bit of that discussed here: https://biology.stackexchange.com/questions/90434/in-the-pr-segment-of-an-ecg-how-come-theres-no-current-flowing/90492#90492

See also https://meta.stackexchange.com/questions/66377/what-is-the-xy-problem

@BryanKrause My question did not ask about the full EKG interpretation because I know it's complex.  I just want to know the total charge that goes through neuron/muscle membranes in the heart for each heart beat (not the directions you point out...it seems like you are pushing this into an xy problem).

I'm trying to figure out why you need this information, though; what do you plan to do with it? That's the XY part. Since you mentioned you were interested in EKG, it seems relevant that answering the question as asked won't really tell you anything about EKG measurement.


text:
Sensitivity Along Digestive Tract
Suppose you swallowed a little capsule with a blunt poker which had
some impulse of force applied every few seconds.  What would be the
sensitivity ordering (of lips, mouth, throat, esophagus, stomach,
duodenum, jejunum, ilium, colon, rectum, anus)?
Does sensitivity just fall to a minimum in the middle of the digestive
tract and increase again to the exit, or are there any other extremum
(e.g., at the ilium-colon interface) along the way?  I'm guessing
people could infer the answer by looking at the density of nerve cells
along this route, but I couldn't find any comparable scientific data
in my quick internet searches.

Let's be clear do you want only perceivable sensibility or non perceivable sensitivity?

I want perceivable sensibility. In the experiment, the person would be ranking how well he/she feels the periodic poking (and for a bonus, I might ask if it feels good or feels painful). It's still subjective, but the best experiment I could think of.

This is such an artificial scenario, I'm wondering why it would matter? Different parts of the GI tract are innervated for different things/reasons.


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Is RGB diode lighting okay for the eyes?
Is a light source giving off light composed of red, green and blue lights harmful to the eyes? Does it lack any important qualities that other artificial light sources, such incandescent lamps or white LEDs may have?
Is it alright to use RGB light panels in a room instead of the usual lighting?

At a fundamental level, no, we're fine with LED lighting.  The absorption spectra of our cones are quite broad, and RGB LEDs are chosen to match our color sensitivity reasonably well.  That red+green looks the same to us as light that is actually yellow is because our eyes can't tell the difference since we don't have good enough spectral resolution in our vision.
There could be more subtle emotional or other complex effects, but to a good approximation, if it looks right it is right, and there aren't magical frequencies that we need to avoid e.g. retinal degeneration or something else awful.  (Well, large amounts of UV are bad, but RGB LEDs don't produce a significant amount of UV.)

Plus, all of the wavelengths in RGB LEDs are also present in white light...


text:
Can gelatine digestion make blood more thick?
Can gelatine cause blood thickening if digested?


text:
Is it ok for Chili pepper plant's fruits to fall into its soil?
I wonder if Chili pepper's fruits which fall into the soil near the plant will harm it, since the peppers are so spicy for people.

The spiciness is because human tongues can interact with Capsaicin - an organic molecule that locks into receptors on our papillae and cause a heat/pain feeling. Not all animals have them, and I doubt the soil would be affected since the seeds - where the highest concentration exists - must be planted. However, I can't look up references right now. :)

As @MCM says, the capsaicin molecule isn't intrinsically damaging - its effect upon us is mediated through the TRPV1 (Transient Receptor Potential Vanilloid 1) receptor in the membranes of cells whose function is to sense noxious stimuli such as heat. The binding of capsaicin to this protein causes transmembrane movement of Ca2+ ions which depolarises the membrane, triggering an action potential - a signal to the brain. Heat has the same effect on the TRPV1 protein. In this way the presence of capsaicin mimics the effects of heat, causing a painful sensation.
Have a look at this SE.Biology question.


text:
What does ophthalmologist see in your eye?
I always wondered what ophthalmologists see inside someone's eye and what they're looking for. The whole thing is a mystery to me. Are there any photos of what the eye of a patient looks like from the doctor's point of view?

Which instrument used by them are you specifically talking about ? Or are you looking for a more generalized answer ?

When he's looking into your eye through his convex reflecting metal mirror with a little hole in the middle thing. I wonder what he sees through it.

That instrument is called an ophthalmoscope. Suzan Cioc is right, they look at your retina.

The name of the instrument is ophthalmoscope. It is used to determine the health status of your retina. Retina is the one of the few places in the body where you can observe the blood vessels directly.
The link also includes a picture of what your eye looks like from doctor's point of view.

They look at retina. Google for it. The look of retina can evident of some diseases. This is the subject of medical education.


text:
Eating rarely but a lot, or often but little
I wonder if it matters if an average person eats the same amount of food distributed between a few (2-3) meals during the day, or constantly having small snacks.
I'm interested in several aspects of such food consumption:

How does it affect appetite?
How does it affect fat accumulation?
Are there any notable side effects caused by either way of eating?

1)Eating little with many breaks is healthy..
Eating rarely but many times increases your fat...
The logic is simple.
Before the Logic..let me shoot a fact.
In mammals: conversion from glucose to fatty acids has a direct pathway(I am speaking biochemistry), but there is no direct path for conversion of fats to glucose..(whereas in plants both paths are direct..)
So If you eat more food at one time, the glucose which body needs is used and the remaining glucose is converted to fat.
when the body again needs glucose, it needs to take a long pathway to convert fat into glucose(* only if you workout), by that time your Hypothalamus gets a signal and you feel hungry. So you again eat to satisfy your hypothalamus and the process continues, with more accumulation of fat in your body.
But in the little meals, there is no accumulation of fat.
2)In either case, the Appetite is affected in the normal and same way.
3)There are no side effects for either pathway, but you have other side effects from the fat accumulated. :P

Can you add some citations? I fear there is little scientific certainty about almost everything in this answer.

I suggest reading Biochemistry pathways. Cannot cite you at one pathway, because it's all interlinked. You learn a lot of facts and understand a lot of human metabolisms, right from why a diabetic guy breath is alcoholic to how proteins build muscle. Interesting stuff.

It isn't about not knowing biochemistry. Please don't be condescending - citations are especially important to prevent misinterpretation by non-experts on health-related topics. There is little to no logic to your answer: stating that it is "simple" doesn't make it correct. A "direct pathway" from fat to glucose is not necessary because animals can use energy sources besides glucose. Glucose is only a common energy source when carbohydrates are being used.

Eating many small meals or eating large meals is irrelevant. The only thing that matters is getting the right amount of calories needed for your body to function properly.
Fat accumulation does not happen if you do not go over your daily calorie limit.
After a big meal your food is not only stored as fat but as a polysaccharide form of glucose called glycogen that is stored in the liver and or muscles for later use.
Therefore, there is no better way to eat, it depends on what size you like your meals to be as long as you stay within your calorie range.
See http://www.choosemyplate.gov for more information.


text:
Is it possible to pet/groom birds?
I wonder if it's possible to pet a domestic crow, or an owl. Do birds respond to grooming as cats or dogs, for example? If so, then how does one pet a bird?

Birds do groom, but not like mammals do. People tend to call their grooming behavior preening. Preening removes dirt and parasites, arranges the feathers nicely, and distributes oils over the feather (very important for waterfowl.)
To answer your question better, we need to look at the specific species. Lots of birds preen each other socially, so if you wanted to pet a bird (in a way it likes) it's good to know how the species behaves.
You mention crows and owls. Crows are social so they may preen each other; they're also sophisticated (cultural) so it's hard to generalize. A 'bird nerd' on YouTube shows convincing footage of such behavior. I think family groups of crows preen each other, but I don't have a source.
Owls tend to be solitary and would not understand preening behavior from a human. A social species of owl might preen; I don't know. Of course, if you just go ahead and pet your owl like a dog, it may appear to like it. It's hard to say if it does like it...it's easy to anthropomorphize a bird with binocular vision!

I know first hand that Diamond, a tame Pionus chalcopterus, will sometimes respond to having his head and neck scratched in an interesting manner: he may make "panting" or "huffing" noises unique to this activity, lean his forehead or beak against my hand, and half-close his eyes.
I'll add to Ryan's answer by pointing out another use of preening: peeling the cover from newly-grown pin feathers.
How to (safely) pet
It's important to read body language correctly. Just as in Manderan it's funny to call your mother-in-law a mountain horse, you must learn the distinction between "scratch my neck" and "stay back or I'll bite".  The ruff is raised normally as a signal of aggression.
Bring your hand up to his level wrist up and fingers trailing down in a relaxed posture. Make sure he sees it, without startling him.  Human hands are not "natural" to non-domesticated species, so give him a few seconds to process.  Higher thinking is slow and an optional "mode" so to speak.  If he wants to be petted, he'll engage or remain neutral and undisturbed.
Diamond has learned through consistancy that a natural but superficial agressive signal is understood as "give me space", so a horizontal body position with beak in-line like an arrow (the "T-Rex position") and a slight (symbolic) darting motion means you should withdraw. But he may change his mind in a few minutes now that the subject has been raised.

The general points are:

understand his body language
be consistent in your own actions and associated meanings. They're learning a pidgeon with you (pun intended), not like dogs that intuitively know humans,
give hime time to "think".
develop a routine


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Why is clownfish attracted to actinia?
I heard that Actinia Equina normally eats what it can catch, but this clownfish here doesn't care much about that:
https://www.youtube.com/watch?v=Ughm4mnZ1ls
Since the actinia obviously can't hold the clownfish, clownfish does whatever it wants with actinia swimming all over it. Is the clownfish having some sort of fish fun, or is there a purpose behind this playing with actinia?

It's an example of SYMBIOSIS
Clownfishes(Amphiprion ocellaris) are never found without an anemone as they have this obligate association with them. Although they can survive without them, but studies show they are much more healthier with than without.
This association is more of a survival necessity. These anemones are actually toxic and the fish is resistance to it. If being attacked they will get inside these and the attacker might be stung with this actinotoxin.
Also,

The presence of an anemone is also essential to reproduction of the
  fishes: their eggs are laid beneath the oral disc overhang of the
  anemone, where they are tended by the male.

Source:

Wikipedia on Sea anemone
INTERACTIONS BETWEEN FISH AND SEA ANEMONES
Clownfish and its mutualism relationship with anemones


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How do birds learn their tunes in isolation from their own species?
I wonder what a bird would sing if it didn't have its parents around (or any other birds for that matter) to learn its chirping sounds from.
I'm interested in how a bird would sing...

in complete isolation from creatures communicating through sound;
in isolation from its own species, but with other birds;
in isolation from all birds (other animals and creatures are there for it)

For example,

Would a bird even feel the need to speak up if there wasn't any other vocalizing creature around?
Would a bird learn other species' signals? Would it only learn from one species, the one which it would think of a fitting mate?
Would a bird try to mimic a non-flying creature's signals?

These are similar questions, but if you think they should be separated, let me know in the comments.

Birds have to learn their song patterns.
They are able to chirp, but the songs with "meaning" are learned from their parents or whatever they learned to be their "parent".
Here is a paper that related bird song learning to human learning (of speech, for example).
Birds brought up by parents from another species learned to sing their songs.
There are many birds that learn to imitate other animals or sounds, so in isolation from all birds they will probably do this.
I can't recall where, but I read a paper once, where little finches brought up by humans developed a song resembling the "Hello there, now there's food", their caretaker always greeted them with. (Not the speech, but the overall sound pattern.) They might not understand the signals, but they try to communicate nevertheless. Some birds use sound from other species to mock others, scare them off or lure them into thinking they might be more powerful than they are.
Birds brought up in total isolation do sing, but not the typical songs you know from their species. Deaf birds who can't hear themselves, though, do not (always) sing.

Nice, thanks for sharing! I was also interested in how birds initially created their species-specific melodies. There probably wasn't someone to teach them, so they must have invented those tunes and then those tunes evolved. Do you know anything about that?

As birds also have regional dialects, the development of their song is part of evolution, like for humans the development of speech, languages and dialects. How that works involves a lot of time and a lot of science I know nothing about. And, I thing the "first development of meaning for a birdsong"-mechanism involves a lot of speculation, too. It might just be similar to development of hindering feathers, that make birds more attractive to their mates. The more elaborate a song, the more effort went into it. So the dads singing songs the mums like got more offspring to teach it to.

this is not true of all birds, yes many birds learn their songs but many birds have completely gene programed instinctual songs. cuckoo's being a classic example. Some will instinctually know a basic song but learn to refine it and make it more complex.  there is a whole spectrum of bird song behavior.


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Why do flies leave dirty spots on shiny/glossy surfaces?
I've seen flies leave dark spots on lacquered wood, mirrors, glass and monitors. Why do they do that? Is it some food stash or are they dumping waste in a single spot? Why pick a smooth surface?

House flies (Musca domestica) prefer to rest on light colored surfaces, and what is lighter than windows, windowframes, glossy surfaces that reflect light, etc.? Where they rest (not eat) is where they defecate (or regurgitate), leaving marks politely called "fly specks".

House flies also leave dark fecal and regurgitation spots on wall surfaces where they rest, and with a preference for resting on light colored surfaces, these spots can be quite noticeable when fly numbers are high.

If you ever visit an "open" barn, you'll notice the phenomenon is quite remarkable. If the number of flies is high, there will be specks everywhere, but the windows and other shiny surfaces will be more densely covered.


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Can you "spam" bird sounds so that birds no longer interpret them right?
Is it possible to make birds confused by repeating recorded chirping or singing? Or do they always perceive them as usual, even if the situation is clearly not as described by those sounds?
For example:

mating song when there's no mate
danger/alarm cries when nothing's going on

Specifically, I'm interested in public placed with a lot of traffic using looping speakers to scare off birds that like to dump upon almost unsuspecting citizens. Like underground entrances and city malls. Does the effectiveness decrease over time because of that?

No idea, but have you thought of the fact that this might scare away those unsuspecting citizens, too?

Yeah, that's quite annoying too. I'm thinking it's not the best solution against birds. But even if I don't have a say in that matter, I want to know more about how it works.

This is entirely anecdotal, but the birdwatching community tends to ask people not to overuse calls (played via a smartphone or similar) to attract birds. Apparently, this can cause birds to stop responding to actual calls in the long run.

This is at least doing some confusion, probably also harm. A lot of wildlife conservationists warn about using smartphone apps which replay bird songs, as they are confusing the animals. An example is the Dorset Wildlifetrust.
This phenomenon has even be analyzed scientifically, and the results show that birds are irritated. Territorial birds seem to be affected more and it has been shown that, when a fake call was replayed to them, they sang more often and longer. In the first paper they speculate that this will drain too much energy and prevent the birds from doing other important things.
The second paper looks at zebra finches, which are not territorial. Here they find that birds pay less attention, the more often the song is replayed.
The articles:

Simulated Birdwatchers’ Playback Affects the Behavior of Two Tropical
Birds
Habituation in songbirds.


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Why do people sleep with their eyes open?
It's a fact that some people sleep with their eyes open, but why does that happen? Is it normal behavior, not a symptom of any sort of disorder? Are there any (dis)advantages to sleeping with eyes open?

Do you have any evidence to support your statements ?

@biogirl I once saw someone do that ;)

Something new for me !I have heard about it only in dolphins:)

I've met a few different people that do this. The most common complaint I heard was dry eyes. I suppose over a lifetime it probably damages the eyes faster, but I don't have any source to back that up, and I have no idea why it happens in the first place.

The medical term is "lagophthalmos" if the person is unable to close their eyes at night.
There are several factors involved, and unless it's due to physical obstruction, lid archetecture (such as short lid length (due to surgery etc)), or facial nerve (CN VII) problems, it's not well understood.
I have seen numerous people with varying degrees of this over the years.  For most of those people, it's an intermittent thing.
Tears are essential for eye tissue health, including cleaning and avoiding infection. People complain of dry or irritated eyes mostly.  But in more extensive cases, keratitis and ulcers can occur, which are bad.  If it's frequent, tell the person to make sure they tell their eye doctor (or if they don't have one, get it checked out sometime) so that the health of their eye tissue can be evaluated.
Another possibility is Grave's disease - in that condition, the entire eyeball protrudes and sometimes the eyelids aren't long enough to cover them adequately.  But what you're describing is probably not Grave's disease.
Wikipedia
American Academy of Ophthalmology


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Is consuming sugar with food as beneficial as consuming glucose (~half of the amount of sugar)?
A few years back I heard at biology class that sugar's molecule consists of half the number of elements of a glucose molecule. So not counting the energy needed to transform two sugar molecules in one glucose molecule, isn't it almost the same (eating N amount of sugar) as eating N/2 of glucose?

You have it backwards. One sugar molecule is equivalent to two glucose molecules, though the actual structure of sugar (Sucrose) is a Glucose + Fructose combination.
While Glucose is metabolized via Glycolysis into two molecules of Pyruvate (which are then used in the Citric Acid Cycle), Fructose enters the Glycolysis metabolism at a later stage as shown here:

The GA-3-P is then turned into 2-Phosphoglycerate and then into 2x Pyruvate.
The end result is that a single Sucrose molecule (Glucose + Fructose) [aka - Sugar] is equivalent to 4x Pyruvate, whereas Glucose alone is equivalent to 2x Pyruvate. Or, if you prefer, a single Glucose molecule results in about 32-36 ATP produced, whereas Sucrose will result in 64-72 ATP produced - with ATP being the primary energy carrier of the cell.

Is consuming sugar with food as beneficial as consuming glucose (~half of the amount of sugar)?
What is referred to in everyday language as "sugar" is sucrose. Each sucrose molecule consists of one glucose molecule and one fructose molecule linked by a chemical bond. These two, glucose and fructose are, in terms of energy value, identical.
Whether they are equally beneficial, or indeed beneficial at all (from a nutritional point of view), is a very big question.
P.S. (in response to MCM):
But... fructose metabolism is largely carried out by the liver. If you are consuming sucrose then the glucose component will raise insulin levels and the liver will be in anabolic mode. The fructose will be converted to liver glycogen via glucose-6-phosphate (as shown in your diagram) and also to triglyceride for export to adipose tissue where it is stored as fat. So the energy yield from fructose will be deferred, whereas the glucose will be used by all tissues immediately.
Later on, as insulin levels fall (and glucagon levels rise) the liver glycogen will be mobilised as glucose for export to other tissues. Some of the triglyceride will be mobilised from the adipose tissue for use as fuel too, but it is widely believed that with a typical Western diet there is a net movement from fructose>fat which contributes to the rise in levels of obesity. Indeed some scientists believe that fructose is the main culprit.

Yes, fatty-acid anabolism is certainly one potential pathway for Fructose. However, the original question was not about typical diets or insulin levels. The original question was directly comparing the potential enegy between Sucrose and Glucose. As you point out, even in fatty-acid anabolism the energy from Fructose is only deferred - not eliminated. Sucrose is equivalent to two Glucose molecules in terms of energy obtained, and I thought the Fructokinase pathway was the easiest way to demonstrate that. :-)


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Does the light color spectrum and frequency matter for photosynthesis?
Do plants grow differently when given sun light, wolfram lamp, fluorescent light, LED light, infrared, ultraviolet, x-ray, unfocused laser and stroboscope?

absolutely - plants are green because they prefer light that is shorter in wavelength than green.  but like the rest of us they would die in quick order in an X-ray!  See: http://biology.stackexchange.com/questions/450/why-do-plants-have-green-leaves-and-not-red?rq=1

It matters a lot.
Take a look at this graph:

This graph is for the "normal" plants containing chlorophyll.
There're also "abnormal" :-) ones, simple water plants and cyanobacteria, that contain various phycobilins for photosynthesis instead of the chlorophyll.
If your question is practical, I'd recommend using specialy-designed fluorescent lamps called grow light.


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What do nerves have to do with feeling nervous?
I was thinking about how when people say: "Nerve cells don't regenerate" (which is, apparently, not true at least for some kinds of nerves) and "You're making me nervous" they might not refer to the same "nerves".
What makes a person "feel nervous"? Does it have anything to do with nervous system?
Bonus question: How did people come up with the thought that nerve cells don't regenerate?

As buzrw's first comment states, most nervousness is primarily a sympathetic nervous system response.
There are also neurotransmitter imbalances involved with anxiety, especially in anxiety disorders.  The NT are dopamine, serotonin, and norepinephrine.
I want to clarify buzrw's comment on nerve cell regeneration, as I am unsure if he is stating it's proven to exist or to not exist.  "Primary neurons are not readily mitotic..." makes me think it's the latter.
Neuroregeneration is proven. Mayo Clinic has good information here and this is a well-phrased simplified answer here.
It is more commonly seen in peripheral nervous system, as the central nervous system has limited capabilities to regenerate.  Mostly it is regrowth of severed axons of  cells, and differs between different nerve cell types.  There are other types of regeneration as well.  They involve many physiological processes we're only starting to understand, such as the role of neuroligin.  Without getting too technical, there is a lot that can be done to help stimulate and guide the regrowth of some neural damage, but there are still chasms in our knowledge in the fields of neurology and psychiatry.

Yes, it's a response caused by a division of the autonomic nervous system, called the sympathetic autonomic nervous system.
Regarding nerve cell regeneration, it's not a thought it's proven. Primary neurons are not readily mitotic.

Could you explain a bit more what is the difference between these nerve cells and primary neurons?


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Why do cockroaches burst from soapy water?
(careful, disturbing!)
I was experimenting with some stray cockroaches that ended up falling in my bath tub overnight (there is currently an infestation undergoing in my apartment building) and I found out that they are very easily killed by simply soaking them in soapy water.
I read that soap blocks some pores in insects' bodies which leads to suffocation, which appears to be the cause of death for my test cockroaches. But what I don't get is why about a half of them died with their innards bursting from their tail end. The water wasn't too hot to make them boil. Is it that they suffocate so hard that attempting to breathe they blow out their insides? Or is it the soap's reaction with the cockroach's bodily materials? Or is something else causing this?
I remember watching a documentary on injecting various insects with hydrogen peroxide which caused much more dramatic explosions, but it's not like I was injecting cockroaches, I just sprinkled them with soap water.

As far as I am aware, cockroaches don't burst from being sprayed with soapy water (water + some liquid dish detergent). We previously had many cockroaches in our apartment (some came back after a year of nothing!), and we regularly sprayed the cockroaches with soapy water plus some vineger (more as a disinfectant/cleaner) and they never burst. We've killed at least 30 using this method.
Having said that, what you likely witnessed was the egg sacs dislodging from the back of the female cockroach. As you didn't mention what species of cockroach you were dealing with, I am assuming you had German cockroaches as they seem to be the most common type in non-tropical/hot areas.
According to a number of biology sites, German cockroaches are particularly difficult to control and eradicate is because they carry their egg sacs with them until they are ready to hatch. At which point they drop the sac.
If you are able to catch a few that seem especially big, you will notice that they have a sac at their back.
If you don't have German cockroaches, I have not idea why they would burst...

What you saw was simply female cockroaches expelling their many eggs as they approached death.
We have German cockroaches here in Australia. I am always astonished at how quickly they spread and equally how easy to is to kill them. While there are many poisons on the Australian market for spraying them, which generally work, often quite slowly, any water which is marginally hotter than what is comfortable to keep your hand in will kill a cockroach in a matter of 10 seconds. If cockroaches are silly enough to be around the kitchen sink, shower or any basin they are very quickly dead meat. Pouring boiling water on them would kill them in seconds.
Many insects will quickly die if exposed to hot water.
I don't like sprays because they indiscriminately kill all insects, good and bad. We have encouraged huntsman spiders in all of the houses we have lived, as they are excellent roaches and fly killers.
But short of flooding everywhere with hot water which isn't a useful plan in most instances, sticky roach baits, which are placed in strategic positions to attract and kill roaches, are the best way to kill (only) roaches over time. They ensure that the roaches get stuck in the bait, and lay their eggs in the bait, thus keeping roach reproduction down.

Cockroach abdomen burst out when it sinks in soapy water. A white color thing burst out from the body which are not eggs.They lay only one big egg which will be in brown color. Cockroach lack hemoglobin(red pigmentation) in their blood. White color busting out is actually blood. So even male cockroach burst out when it is in soapy water. May be due to some soap reactions with blood it burst i guess.

Can you add some references please?


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Physiological or molecular difference before and after sleep?
I know that the details of the process of sleep aren't entirely known, but have always wondered why I feel rested after sleep.
Biologically, what differences can be directly observed in the human body before and after a good night's sleep?

Can you be any more specific? Sleep affects every single organ and organ system in the body, and everything from hormone levels to cytokine levels change from tissue to tissue based on the amount of sleep you get.
Your question is almost impossible to answer concisely.

Similar: http://biology.stackexchange.com/q/3028/6422

The simplest answer is adenosine binding. Throughout the day, molecules called adenosine bind to specific receptors and as more and more of these accumulate, you feel more and more tired. While you sleep, these connections are broken and when you wake up in the morning most of that adenosine has been removed from the receptors and you feel well rested and less drowsy. As a bonus fact, caffeine is shaped like adenosine and the reason caffeine works is that it can bind to the same receptors and thereby prevent adenosine binding and prevent that feeling of drowsiness to set in.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769007/


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Is human face more resistant to cold than other body parts?
Walking outside tonight in -15˚C I realized an interesting observation: While I felt cold on most part of my body, my face (although the only uncovered part) didn't really feel cold. It registered the temperature of course, but it wasn't a negative perception.
I wonder, what is an explanation? Is it simply because our faces are used to the cold, because we almost never cover them? Or is it some evolutionary phenomenon?

I think you should try to measure the temperature of the skin on your face vs. exposed skin elsewhere to determine if the difference is real or perceived. The head receives a disproportionate amount of blood flow when cold, associated peripheral vasoconstriction. So the extra blood could actually be keeping your face warm. Or it could just be a perception of warmth.

specific body parts are adapted to be heat radiators and so have a different role in heat regulation.  i think for humans its the pads of the hands.  http://biology.stackexchange.com/questions/5449/what-is-the-evolutionary-rationale-for-palm-sweating/5464#5464

After 30 years of working outside year round I can verify that my face and hands especially stay far warmer. I can work in freezing temps without gloves without any issues. Right now the blood vessels in my hands are so dilated after spending several hours inside that my hands feel tight ( spent 10 hrs outside working, no gloves at -5 c today) . Short answer is your body is very adept at adapting to the environment .

In response to cold your body causes blood supply to the skin to drop in the whole body. This is to conserve heat, but results in us feeling really cold. Exercising reverses this, resulting in an increased blood supply to the skin in order to remove excess heat and in this case we feel hot.
As mentioned, the head receives a large blood supply, and continues to do so despite other tissues being restricted. This is particularly as a result of the brain requiring a lot of oxygen and glucose. This keeps our head warm.
This phenomenon is why hats keep us warm and are important in cold weather, we lose a lot of heat from our head.
It is also likely that the skin on our head contains less cold receptors, as these aren't likely to be required. However the other parts of our body, particularly the soles of our feet and anterior surface of our hands have many sensory receptors. They are likely to make first contact with anything that may be harmfully cold.