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How to determine the probability that a mutation is lost / fixed?
I have a question about how to determine the probability that a mutation is lost or fixed after 1 or 2 generations in population genetics.
Let's say we have a randomly mixing population, with N diploid individuals (N=5), and there is one mutation that appears. I know it should follow a binomial distribution, but I also heard it may follow a Poisson distribution... and all I feel like saying is that the probability to get fixed is the same as the frequency at time 0, which is 1/2N, or here 1/10.
Furthermore, how do you calculate the probability that it exists in 2 copies?

your question assumes that a mutation is something that is "broken" - might want to reword a bit

Thanks a lot for your reply ! It helps a lot. However, shouldn't we use 10 among 2, instead of 5 among 2 in the binomial calculation, as we're looking at alleles in a diploid population ?

@VanceLAlbaugh 'fixed' is a technical term in population genetics. It has nothing to do with a mutation being 'broken'. Fixation is when a mutation reproduces through a population until  essentially 100% of the population has the mutation. Loss is the opposite process, where a mutation disappears from a population. Fixation and loss can be entirely chance processes, or they can be driven by a selective advantage or disadvantage of the mutation.

@CharlesE.Grant excellent - thanks for clarifying... might want to edit question to clarify that - as users unfamiliar with that (like myself) clearly interpreted that differently

How to determine the probability that a mutation is lost / fixed?

The probability that a neutral mutation gets fixed after an infinite amount of time is equal to its frequency $p$ as you said. Therefore the probability of being lost is $1-p$. This post offers an explanation but there many ways to make the demonstration. You might want to have a look at any good book in population genetics for this demo. Here are book recommendations.

how do you calculate the probability that it exists in 2 copies?

A probability always depends on a priori. What are your a priori? Let's assume that we know that the allele frequency was $\frac{4}{10}$ in the previous time step.
Under the Wright-Fisher model the probability of having 2 copies in the next generation is given by the binomial distribution. Let $N=5$ and therefore $2N=10$ and let the frequency of the allele of interest be $\frac{4}{10}$, the probability of having two alleles in the next generation is ${10 \choose 2} \left(\frac{4}{10}\right)^2 \left(\frac{6}{10}\right)^8 ≈ 0.12$.
Under the Moran model this probability is zero. Moran's model is a birth-death  model (Markov model) and therefore transition between time steps can only add or subtract (or make no change) a single allele. You will note that the time step does not mean the same thing for the two models. Loss of heterozygosity is twice as fast under the Wright-Fisher model but this discussion is definitely not what you were asking for!

@user27813 Thanks for your comment. You are right, you said diploid population with $N=5$ and I considered a haploid population in my answer. It is fixed now.

If you know the probability of an individual surviving, both without & with the change, you can calculate the probability of the gene surviving. This isn't actually knowable, so the details of the model used to estimate seem inescapably relevant to any answer to me. Am I missing something, here?

@TheNate I don't really understand your comment. Typically, what do you mean by "the change". These models are models of genetic drift, they assume all individuals have the same fitness. The probability of an individual to produce k offspring is given by a poisson distribution with rate \lambda=1.

"The change" I meant was the mutation of interest. I understand/understood what the models represent; you answered the question. That set of (apparently customary?) simplifying assumptions is exactly what I was missing.


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Principle of 16 S rRNA technique for bacteria identification
Why do we isolate DNA not RNA in 16 S rRNA technique for bacteria identification?

Please ask only one question at a time. Your other questions have already been answered here and across the web. Please do your own research before asking.

There are several reasons some of which are fairly obvious:

The most obvious reason is that PCR only works with DNA, because it uses DNA-dependent DNA-polymerase. One can argue that you can use an RNA-dependent RNA-polymerase, but it has several drawbacks, mainly the cost and synthesis accuracy (Lauring et al., 2013, Nature). Since RNA-polymerase itself has higher error rates than DNA-polymerase (Berg et al., Biochemestry 5th edition, 2002) RNA transcripts might already have some variation from the original gene and using a low-fidelity polymerase in PCR will only lead to exponential error accumulation, which reduces identification resolution.
RNA is less stable in aqueous solutions due to the additional -OH group at the 2' position in the ribose, hence RNA extraction and storage is more complicated and expensive in most cases.
In community studies DNA and RNA have different biological implications, hence metagenomics and metatranscriptomics are different fields.

There are several issues with this answer. (Point 1) RNA sequencing is cheap, easy, and very accurate nowadays. cDNA conversion of RNA, also known as reverse-transcriptase RCR, has been common for quite some time now, with highly accurate RTases being used from many different suppliers. A study from 1988 about HIV is not very current evidence of your thesis, especially in the incredibly rapidly-changing world of mol bio. (Point 2) RNA-Seq instruments are provided by a number of companies, and they all work (initially) with RNA. It is also possible through a variety of methods (...)

(...) to get quite good results using nanopore sequencing nowadays. (Point 3) the second part of the sentence is just wrong. Take a sample, throw it in RNeasy, and store it in the freezer indefinitely. Buy a cheap (depending on your budget) Qiagen spin column, purify the RNA at your convenience, aliquot, and store indefinitely at -20 or -80. Cheap and easy. I'm not sure what the point of Point 4 is.

@MattDMo thanks for your feedback. 1. I removed the revertase-related statement, though I've found no papers comparing error rates of high fidelity DNA-polymerases and high fidelity revertases (it would be great to get one from you); 2. I've been unaware there are machines, except for nanopore, that directly sequence RNA; as for nanopore, although huge improvements have been made, I haven't seen any reports with accuracy > 0.9 (which is laughable when we speak about identification). 3. I've used that kit myself, that's why I wrote that RNA extraction is more complicated and expensive...

... As with RNA-sequencing, I haven't written that it is impossible or something, I've only said that it is more expensive and complicated than DNA-sequencing. And when you only need to identify something, you go for the cheaper and simpler solution, given equal precision; 4. in community studies RNA-seq is commonly used to distinguish active and dormant microorganisms (though it is a complicated theoretical issue), while DNA-sequencing is used to assess structure and composition at the highest possible resolution; DNA-seq usually uncovers more diversity.

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What is the primary function of a leaf?
The Wikipedia article (https://en.wikipedia.org/wiki/Leaf) gives the usual view:
'A leaf (pl.: leaves) is a principal appendage of the stem of a vascular plant,[1] usually borne laterally above ground and specialized for photosynthesis.',
with the article on photosynthesis (https://en.wikipedia.org/wiki/Photosynthesis) launching into an explanation of the capture and conversion of light energy into chemical energy stored as simple carbohydrates. In this view, light harvesting and energy conversion is primary.
However, the energy efficiency of photosynthesis is only about 0.1-4.3% (https://en.wikipedia.org/wiki/Photosynthetic_efficiency). If light energy capture and conversion is primary, why is the efficiency so low, especially since there seem to be some obvious ways to improve efficiency, such as increasing chloroplast density or recruiting different pigments to increase the number of usable frequencies of incoming light?
But photosynthesis requires water and carbon dioxide as well as energy to function. From the Wikipedia article:
$$
6~H_2O + 6~CO_2 + Energy \rightarrow C_6H_{12}O_6 + 6~O_2
$$
With water relatively abundant within the plant, the limiting factor would seem to be rate at which carbon dioxide can be extracted from air. Its concentration there is currently only about 430 ppm, and it was considerably lower in the recent past.
Could it be instead that leaves are structurally optimized mainly for carbon dioxide extraction, with light harvesting secondary, only just enough to process the resulting carbon? Is there any evidence for this?

I think that's an inclusive "and" in the first quote - to reword Usually specialized for photosynthesis and borne laterally above ground. Meaning that the specialization for photosynthesis isn't always a feature of leaves. IMO transpiration is far more important to the plant than photosynthesis

If you go to the "Typical efficiencies" section of the Wikipedia article you link, you'll find a breakdown of the inefficiencies of photosynthesis in plants, which states that only 30% of usable light does not hit chloroplasts. Therefore, even if 100% of usable light hit chloroplasts, efficiency would only be about 40% higher - which is a lot, but still leaves us in the 0.1-10% range. Chlorophyll also requires a ton of nitrogen, which is very often limiting to plant growth, so it might not be beneficial to add more chloroplasts for diminishing returns in photosynthetic efficiency.

In terms of recruiting different pigments - plants already do. Plant photosystems include a number of accessory pigments, which absorb wavelengths that chlorophyll a can't and fluoresce wavelengths that it can. Many algae have additional pigments that plants don't, which may just have happened to arise in algae but not plants.

@Eonema Not to mention the waste heat disposal from absorbing all the light and fixing the CO2 to sugars.

@Eonema I am aware that plants already use other pigments. They could presumably use even more if energy use efficiency was a big problem. The point is that extra energy would simply be wasted if there wasn't enough carbon to convert to carbohydrates

I would consider that photosynthesis as a term includes both the process of light harvesting and the process of carbohydrate anabolism from CO2. I don't see any tension in the definition that you've quoted. None of them is exhaustive and none of them is exclusive. Many leaves have minimal roles in either process and have been adapted to other purposes- for example parasitic plants that do not rely on photosynthesis! Biology is messy and that's ok.

Plants need to both capture carbon, and capture light energy to store it in carbon bonds. Since plants use CO2 as their carbon source, but can't store CO2 directly, carbon capture and photosynthesis are intimately linked. In my opinion, it doesn't really make sense to distinguish between photosynthesis or carbon capture specialization.
That said, plants have many adaptations around gas exchange. Although water is used directly in the photosynthesis reaction, the main loss of water is in the gas exchange itself. Essentially, whenever the stomata (the structures on a leaf surface that open/close to allow gas exchange) are open to accept CO2, the plant is also losing water through transpiration. Despite OP's assertion that water is abundant within a plant, most plants need to tightly control their water budget, as they will generally face water scarcity at some point in their lives.
Off the top of my head, an adaptation for increasing the gas exchange is the structure of the spongy mesophyll, which has space between the cells allowing for air exchange through the stomata. Plants have many adaptations to increase water use efficiency. Two of the primary ones are C4 and CAM photosynthesis, which separate carbon fixation from the photosynthesis reactions either physically (C4) or temporally (CAM).
Alternatively, low-light plants do have adaptations to improve light gathering, especially for light that has been filtered through leaves of an upper canopy. Plants adapted to low light may adjust the stoichiometry between photosystems I and II to better take advantage of far-red wavelengths passing through other leaves.
Because of the interplay between light, water, and carbon in photosynthesis—and the extremely varied environments that plants inhabit—I'd say that declaring that leaves are "specialized for photosynthesis" naturally encompasses a specialization for each of these resources, tailored to the habitat (and micro-habitat) of the species.

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Identify snails
Can you tell me what are these 2 kinds of snails I found?
The first is around 2cm shell diameter. The second is around 3cm shell diameter.
I found both of them in Normandy (north of France) 100km from the sea, and found 2 days ago (summer).

I've just edited the post

The first one is Cepaea nemoralis, the Grove snail, one of the most common snails.

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What is the name of this species which I found in an Epipremnum (Money Plant)?
I found a very rare specie (at least from my knowledge of species and research) today in a money plant (Epipremnum plant) in my kitchen garden. This caterpillar was on it. Please help me with the name of this species and any information about it.

Can you add size and location?

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Why do we perceive colour? (i.e., distinct values?)
This is a question I often asked myself, but never really found a satisfactory answer to. It may be that I always went about it from a wrong starting point because the question is induced by physics. But I think an evolutionary perspective may be the most satisfactory one to explain this.
Humans and other animals had much to gain from differentiating not only dark and light but also colors to identify edible things, or threats etc. For this purpose we developed multiple types of cone cells. But what reason is there to not perceive light as we perceive sound, in a spectrum? We could easily distinguish said things by just knowing how high or low the light frequency is (or for that matter, what the spectral 'fingerprint' of specific objects is). Why differentiate between an - albeit big - array of colors?
Or, to go one step further, why did we need an extra type of cone in the middle, the yellow-green wavelength? Is there an evolutionary reason? I'd settle for using the three more or less distinct cone sensitivities as explanation that the brain just has enough information to arbitrarily differentiate these into very discrete cognitive signals.
But evolutionarily, there has to be a purpose, so that one of the questions is the right one. The colors must bring something to the table. Or not?
Thanks in advance. I am also grateful for anyone nitpicking my arguments, because it always helps.

"But what reason is there to not perceive light as we perceive sound, in a spectrum?"

We do perceive light in a spectrum. Not just in a spectrum, but in a combination of spectral components (because we rarely in nature observe true single-wavelength light). If you are thinking about names of colors, those are just words we made up to describe colors to other people, and the range and spacing of those colors differs across language groups. We do the same for sound in the context of music: B-flat versus an E, for example.

Or, to go one step further, why did we need an extra type of cone in the middle, the yellow-green wavelength?

Colors are perceived in vision by the ratio of activity of different cones, and intensity and spectrum can be confused. If you have no "green" cones, there are big stretches of wavelengths that only activate one of the other two cones. In that situation, there is no way to discriminate between intensity and color.
If, on the other hand, you are wondering about transduction, it's because sound and light have different physical properties. The cochlea effectively "maps" sounds onto a physical arrangements of hair cells. You could do something similar with a prism, but you would lose spatial acuity (effectively, you would need a whole spectrum analyzer for the receptive field of each photoreceptor: your retina would have to be absolutely massive). Instead, color vision works by differential chemical sensitivity to different light wavelengths.
Your question doesn't seem to be much about evolution, besides the title, so I left off that part.

Thank you, the prism idea makes perfect sense! Eyes are very much made for spatial resolution and then there is a trade-off there. But I don't buy what you said about intensity vs. frequency perception: If the brain had no way to differentiate, wouldn't that be the case for three cones too? Mathematically, I can extrapolate from two received signals and 'map' an intensity curve over color values 'given' by my reception, to adjust for the 'blind' spot. The blue and red cone even overlap in their spectral range, if I'm not mistaken, so in principle there is no problem there, right?


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What is the name of this plant with Fig-like leaves & mulberry look like fruits?
Location: Napa, California
Size: It's 20' tall now.


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clades on a tree - biopython
Suppose we have an alignment. When a phylogeny tool (PhyML in this case) is used on this alignment, a tree consisting of 5 clades is returned.
The thing is: suppose we have this alignment on a web site, and some user uploads a new sequence to add to this alignment. After realign with the new sequence, phylogeny inference is applied, and then, a tree visualizer.
I'd like to know which one of the 5 clades contains the new sequence (if any), without the need of looking at the tree.
How should I approach this issue? I think that first of all, I should define my clades (how to?), and then, measure distances from my new sequence, to all clades, and keep the one with the shortest distance...But I'm not sure if this is a good strategy (not to say I'm not sure how to accomplish this..)
This is maybe more of a concept question...
I'm working with biopython.

Welcome to BiologySE... thanks for your question. Do you think this is more of a programming question? If so, you may want to ask it on another SE site. Also, check out the help page for tips on how to ask a good question - you may want to edit and/or revise what you have to improve it. See this link: http://biology.stackexchange.com/help/how-to-ask

You could decide to just insert the new clade next to some "closest" one ("closest" being defined in a clever way that remains to be devised), but it is possible that the result will be different from what you would obtain by reconstructing the phylogeny from scratch. The reason is that the information that the character combination in the new clade brings may alter the relationships between the other groups present in the data in a newly optimized phylogeny.
An example of application is that one typically wants to add more taxa in a phylogeny in oder to prevent long branch attraction.
As an aside remark: When one speaks of a "clade", one usually thinks of a bunch of terminal taxa (leafs of the tree): do you want to insert an whole bunch of taxa forming a monophyletic group, whose internal topology is already known, or just one terminal taxon?


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Do animals have the notion of fair share and fractions?
There are already several experiments showing that animals (not only humans) can do some math: counting and problem solving.
My question is: what about the notion of fair share and fractions? I am looking for any reference or study!

Welcome to the site. Please take a [tour] and visit the [help] for more information on the Biology Stack. Please note the homework policy. So - what have you found in your searches, and what do you mean by "animals" - note that we are animals, as are insects, fish, birds, primates, other mammals...

please take a look here https://www.youtube.com/watch?v=meiU6TxysCg


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Griffith's Experiment Conclusions
My teacher gave us these two questions on Griffith's experiment.

How did Griffith's experiment rule out that the rough cells could have used the capsules of the smooth cells to become pathogenic?

Why did Griffith know this experiment was important?

They said the answers were that

If they incorporated the broken capsule, then the next generation will not have the capsule, that's why we know it wasn't the capsules that made the rough cells pathogenic.

It ruled out proteins were the genetic material.

My problem with these answers is that it relies on knowledge we know. For the answer to number 1, the capsule could have contained genetic material and passed it on to the daughter cells (we know that isn't true but they didn't know proteins weren't the genetic material back then). I don't think the experiment ruled out the capsules were the factor making them pathogenic at all. I feel like all the experiment proved was that bacteria could transform. Beyond that, from my understanding, it didn't prove nor rule out what was leading it to transform - whether it was through protein or DNA.
What am I missing here? If my teacher is incorrect, what should I put down?


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Bacterial division and mutation rate
When a bacteria A divides it produces two cells A', A''. Each of them receives a copy of the chromosome/plasmids. Now, DNA replication occurs way before division in a semiconservative manner. That is, each new chromosome has an 'old' strand and a 'new' strand. Since the polymerase is error prone, my belief is that both genomes can potentially have mutations. Now when people refer to the mutation rate/genome/replication, e.g. 3x10-4 , Does this mean that:

Only one of the resulting genomes have this mutation rate? (according to me not likely).
The mutation rate takes into account the total number of mutations in both new genomes.
Each of the genomes can potentially have independently as many mutations as the mutation rate specifies.

i'm referring to replication erros, and not the two strands in a single genome, but to the two new strands in each of the two genomes.

edit of previous comment: I believe it would be option 2 or 3 depending on what sort of error has occurred and when - i.e. if there is damage to the old strand it could affect a strand of dna in both cells, if it is a transcription error in the new strand it may only affect a strand dna in one cell (A') and the A'' cell may be identical to the parent... (just a quick estimate at an answer)

Your question comes down to the definition of the units you state in your question - mutations genome-1 generation-1. In my opinion the answer is your choice (2).
How are mutation frequencies measured? Usually it is a case of scoring the appearance of a mutant phenotype as an indicator of underlying mutational events (see Drake,JW (1991)A constant rate of spontaneous mutation in DNA-based microbes. Proc. Natl. Acad. Sci. USA 88:7160-7164 for a detailed explanation.) Since, as you say, DNA replication is semi-conservative, the two daughter cells of a bacterial cell division each inherit one old DNA strand and one new DNA strand and so have the same probability of sustaining a given mutation. The overall mutational frequency has to be an aggregate of what has happened in both of them (and in all other cells in the population) since there is no way of distinguishing between them. In terms of your question the answer is (2) and this is why the mutation rate is normalised per genome.
In practice this figure is arrived at as follows. Suppose that you study a 1 kb gene, gene X, and measure the rate of spontaneous mutation in that gene (by some convenient assay) as 1 mutation per 107 cell divisions (again see the Drake reference for details). Assume also that the bacteria have a genome size of 2 x 106 bp.  Since each cell division equates to the creation of one new genome we get:
mutations per gene X per generation = 1 x 10-7
mutations per bp per generation  = 1 x 10-7/1000 (because it is a 1000 bp gene)
mutations per genome per generation = 1 x 10-7 * 2 x 106/1000
mutations per genome per generation = 0.0002
Now this is an underestimate because not all mutations will create a detectable change in phenotype. Drake uses a correction factor of 3.12 for this.
true mutations per genome per generation = 0.0002 * 3.12 = 0.0006 or 6 x 10-4
These were made-up numbers. See review in Drake JW et al.(1998) Rates of spontaneous mutation. Genetics 148: 1667-1686 for real examples.

Sorry for being so dense i think i understand why the rate is normalized by genome, but then can i say that daughter A' has N mutations and daughter A'' M mutations, then can i say that both N and M are distributed as a poisson variable with the mutation rate as the lambda?


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I hit an area of my elbow and had a burning sensation throughout my hand
I happened to bump the side of my right-hand elbow on a corner and suddenly felt a burning sensation on the right side of the hand elbow-up. Any theories that could describe what I recite?

While this sounds like you hit your ulnar nerve, it also sounds like a question about personal medical health which are generally considered off-topic on this site.

Ulnar nerve supplies sensory innervation to medial 1.5/5 of the hand(i e. Medial 1.5 digits). So when you hit your elbow, ulnar nerve is involved (it runs over medial epicondyle of humerus). So there is a kind of burning sensation felt.

It's often referred to as hitting your funny bone:
Heres one reference on the subject:
https://www.huffpost.com/entry/hitting-your-funny-bone-i_b_12201698
and here is another:
https://www.mentalfloss.com/article/21474/what-funny-bone-and-why-does-hitting-it-hurt-so-much#:~:text=When%20you%20hit%20your%20funny,the%20ring%20and%20pinky%20fingers.
The ulnar nerve is exposed near the bones of the elbow, especially if the elbow is bent. You can probably locate it with your index. If you hit the ulnar nerve near the elbow, it can be felt in the little finger and one side of the hand.


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Why does the sweat of children not smell like adults?
My kids sweat plenty in this hot heat, but they don't smell afterward. I on the other hand need all kinds of deodorant. Why doesn't kid sweat smell?

There are two types of sweat glands: (1) eccrine sweat glands and (2) apocrine sweat glands.

Eccrine sweat glands are present from birth in humans and secrete sweat that is mostly water and functions in evaporative cooling.
Apocrine sweat glands are found in the armpits and groin regions and become active in humans at puberty (although the distribution appears to be broader fetally). These sweat glands secrete an oily substance containing lipids and proteins that through interactions with bacteria on the skin (e.g., bacteria digesting lipids), lead to the "smelliness" of adults (including body odor).

So it's not really the sweat that smells, it's the action of bacteria on apocrine sweat that becomes prevalent after puberty.

Excellent, thank you! I did know that the smell comes from bacteria, not the sweat, but I didn't know we had two kinds of sweat glands. Darn those apocrine glands!

Which leads to the natural question, why are those second category of glands active only after puberty?


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Is there any recent evidence for the aquatic ape theory of human evolution?
The aquatic ape theory suggests that many features that distinguish humans from their nearest evolutionary relatives emerged because the ancestors of humans underwent a period when they were adapting to an aquatic or semiaquatic way of life, but returned to terrestrial life before having become fully adapted to the aquatic environment.  Is there any new evidence of this?

interesting - I have not heard this theory. Did you have links/references to this from your own reading?

There is a book called "Aquatic Ape Hypothesis" by Elaine Morgan which is definitely worth a read.

I'm very interested in this too. David Attenborough once did a radio programme about the aquatic ape hypothesis, and you can listen to it free online.

In short: No. http://johnhawks.net/weblog/topics/pseudoscience/aquatic_ape_theory.html

See also: http://www.aquaticape.org/whyanthro.html

The johnhawks.net article is not a good piece, being poorly written and poorly reasoned. On the other hand the http://www.aquaticape.org site is very well argued, but has no references.

maybe we can close this question at this point? can one of you someone write up what the above to get this off the books?

The Aquatic Ape theory has never gained wide acceptance. This is because it has never had strong evidential support.
The features supposedly supporting the hypothesis only do so under an extremely superficial analysis (e.g. the argument for bipedalism), frequently actually occur in other non-aquatic mammals (e.g. hairlessness in naked mole rats and rhinos, a descended larynx in red deer), show no sign of having arisen at similar times in the human evolutionary record (e.g. encephalisation evolved far later than bipedalism and bipedalism vastly predates hairlessness) and lack fossil evidence of having evolved near aquatic environments.

yes - An idea is often not a hypothesis, and hypotheses often have no supporting evidence.

Article in the Guardian by an Editor of Nature on this: http://www.guardian.co.uk/science/occams-corner/2013/may/07/aquatic-apes-creationism-evolution  I wouldn't say this theory is creationism, but it does not have the weight of any evidence behind it, which is necessary for evolutionary theories.


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How does skin healing work?
I stacked my bike and split my head right open.  About three weeks later the scab falls off and the skin is sealed over, like magic!  How does it all work?  How does the brain know that part of the body is injured and needs repair, or does the brain know at all?  What kind of signals between brain/cells/body are involved.
Sorry it's probably a basic question for a biologist, but I come from a different field and have always wondered about this amazing process.  It's also a very hard topic to google about, because most results are about spiritual healing, crystals, prayer and a lot of pseudoscience rubbish.

There's a WP page at http://en.wikipedia.org/wiki/Wound_healing , and I'm pretty sure that your brain has nothing to do with it.

Healing in the body is normally independent of the brain. Following an injury, a process of inflammation attracts lots of cells to the site of the injury (including platelets, white blood cells, clotting factors). There's also vasoconstriction (tightening of your blood vessels) to reduce blood loss from the injury site. Your skin cells continue to divide rapidly until new skin replaces the damaged one which later falls off. This is a highly simplified version of the process but hope it makes sense. So in summary, healing takes place by cell division (also known as mitosis).

Amongst other things, contact inhibition is also important to stop the cells from over-proliferating.

Hm, do you think that is also possible explanation of the kind of placebo case with soldiers whose injuries healed more slowly if was stressed? How brain tightens the blood vessels?

aha, http://www.dana.org/Publications/ReportDetails.aspx?id=44313 says something quite different


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Are there any mammals in which polyspermy produces viable zygotes?
Are there any mammals in which polyspermy produces viable zygotes? In the wikipedia page it is mentioned that there is a delicate equilibrium between female defenses against many sperms, which ocassionally results in low fertility rates (which in not all cases might be an evolutionary disadvantage, but i disgress)
My question is if there are cases where a ovum can be fertilized by several sperms, and the zygote somehow manages to select fairly between a subset of all chromosomes, avoiding polyploidy and producing a viable embryo.

The short answer appears to be "no".
The longer answer seems to be dependent on what you mean by "viable". Triploid humans do exist that apparently arise from dispermy, but most such fetuses die shortly after birth. Those that do not die soon after birth have a variety of health issues such as intellectual disability; "The few [triploid] infants that do survive to term have multiple severe birth defects." They're almost certainly sterile, though that source doesn't say anything about it.
The existence of elaborate physiological mechanisms for blocking polyspermy in sexual organisms generally, and further mechanical means for limiting sperm number in mammals, argue that polyspermy is something that we spend a lot of effort because it's bad. Here is a recent review of polyspermy in mammals; it has a lot more information about both mechanisms and statistics on the outcomes of dispermy.


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In which month should I map maritime vegetation?
I'm studying habitat use by Brent Goose in the UK, a species that feeds on maritime vegetation. It's main food types are Zostera sp., Ruppia sp., Ulva / Enteromorpha sp. and Puccinellia sp. I plan to map these vegetation types on an inter-tidal mudflat in North-east England during the summer.
I want to choose a month to map these vegetation types that will allow the most accurate mapping of their distribution of vegetation across the mudflat. I think there are two considerations 1. the month they easiest to identify 2. the month they are most visible.
Which month should I choose?

@kmm. Thanks for edit. What do asterisk around Enteromorpha mean?

That's just the markup for italics. For some reason the parser didn't like /*. I added spaces around / to make both genera italics.

One way to approach this problem would be to look at herbarium collections of the taxa that you're interested in. Usually, a flowering or fruiting specimen is easiest to identify; but no matter what character is best for your taxon, if you look at the herbarium collections and see that
-most of the collections identified to species, or
-the especially good-looking collections, or
-flowering/fruiting collections,
were made in a certain month or season, that could help you to narrow down your time window.
As a bonus, in reviewing herbarium collections, you'll have given yourself a step towards being able to identify the species.
Some herbaria have some collections online; here, for instance, are records and images for online Puccinellia collections at a number of UK herbaria.


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Does retinal detachment happen more frequently at night?
My understanding and experience is that during the night photoreceptors are less tightly coupled to the retinal pigment epithelium.  Does this make it more likely for a retinal detachment to happen at night?

In case of normal, healthy person, no, I don't think so. In fact, retinal detachment could happen at anytime of the day. Main causes are diseases and illness, such as AIDS, diabetic retinopathy, cancer, or trauma such as post-cataract surgery and being hit/kicked hard on the eyes.


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What's the smallest organism that can produce voice?
What's the smallest organism (animal, insect, or any living creature) that can produce voice. And not just make sound, but has an organ to specifically to create sound, like how us mamals have vocal chords.

How do you differentiate between an animal that makes sound and one that has a sound-producing organ? If a beetle makes a sound by rubbing its wings together, it has a sound-producing structure, does it not, even if that structure is not dedicated to only making sound?

@MattDMo Does it know it's producing the sound, i.e. is there a purpose for it do make sound, or is it a by-product of rubbing its wings?

would you consider ultrasonics as voice too?

@WYSIWYG Sure, sound is sound. Although, if it doesn't become "too broad" of a question, the best would be an animal from each of both categories.. (or all three if infrasonic is also considered)

I rolled back the question to the original, which is not a duplicate.

I will go with lesser water boatman(Micronecta scholtzi).
The loudest of everything as well as small.
Size: 0.07-inch (2-millimeter)

Produces the highest sound by size ratio.
It's sound is almost equivalent to pounding jackhammer at two feet distance.

http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0021089.g001&representation=PNG_L
Source and Image Courtesy:
So Small, So Loud: Extremely High Sound Pressure Level from a Pygmy Aquatic Insect (Corixidae, Micronectinae)
Youtube: https://www.youtube.com/watch?v=i7-hREXmMFM
Update:
If we consider voice, I will go with Paedophryne amauensis

Smallest frog an known vertebrate
size: 7.7 mm (0.30 in)

I'm putting my bets on the Pistol Shrimp (Alpheus heterochaelis)
They can be grow 3cm to 5cm Long which is incredibly small for the amount of db it can create.
Their sound is a by-product of their large claw snapping shut and creating a cavitation bubble that creates a lot of pressure and then produces up to a recorded 218 Decibels.
This "click" or "pop" of the bubble only lasts less than 1 millisecond. It also produces around 5000k in heat from the popping of the bubble.
(According to the Daily Mail which I honestly may say is probably not the most trustworthy source of accurate information http://www.dailymail.co.uk/sciencetech/article-1085398/Deadly-pistol-shrimp-stuns-prey-sound-loud-Concorde-UK-waters.html
Wikipedia Article : http://en.wikipedia.org/wiki/Alpheidae )

Wow! Watch them in action.


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Usage of the taxonomic classification "Pinnipedia"
According to ITIS the classification Pinnipedia is  invalid, and it is proposed to rather use Caniformia. The later group however includes a range of terrestrial animals as opposed to the pinnipeds (the seals), which only include marine mammals.
Is the term Pinnipedia nevertheless still accepted and used in scientific media? Is there any debate whether to use one and not the other?

The Comments section of that page has the explanation:

Wilson & Reeder (eds., 1993) note that "the pinnipeds (otariids,
  odobenids, and phocids) are included within the suborder Caniformia;
  placing them in a separate Order would make the Carnivora
  paraphyletic." This arrangement continues to be followed in Wilson &
  Reeder (eds., 2005)

If both Carnivora (Bowdich, 1821) and Pinnipedia (Illiger, 1811) are orders in the traditional Linnean taxonomic sense, then one cannot be nested within the other. If this were to happen, then Carnivora would be paraphyletic because it would exclude some of its members. The same argument is made when discussion birds as dinosaurs (you can't talk about Dinosauria that doesn't include Aves).
The problem arises when phylogenetic systematics (clade names) meets traditional Linnean systematics (orders, suborders, etc.). Phylogenetic systematics does not distinguish these higher taxonomic groups. Clades are just nested groups of monophyletic taxa.
So then to answer your last question, Pinnipedia does appear to be in common usage (Google Scholar reports several hundred citations in the past few years). The key is to distinguish Pinnipedia as a traditional Linnean order (not valid) and Pinnipedia as a monophyletic clade that includes seals, walrus, and sea lions (perfectly fine). Seals, walrus, and sea lions are all more closely related to each other than to other Carnivora, so they are monophyletic, and the name for that grouping is Pinnipedia.
Here's the Tree of Life page that has all the clade names.


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Deterministic model of lambda-phage lysis/lysogeny [MATLAB]

Project 1 Base:

Can someone please help me understand what I need from Project 1 Base code to do questions 1 and 2 from the first image? I'm new to MATLAB so a thorough explanation would be great.

This can be done using loop method or Forward Eular's. I don't know which one is easier for this question nor would I know how to do it myself since I have never taken a programming course before and am somehow expected to know how to do all this.

For homework questions, the policy is to see some work from the poster.  Since you don't know programming, I've outlined what the code is doing, beyond the simple operations (+, -, /, *, ^), to get you started.  I think you should be able to implement the models with this information, and I'd be happy to confirm your own answers.

So the best way to figure out what any line of code means, in any language, is to type it and see what happens. To help you get started with programming in MATLAB:
Any text following a % (on the same line) is a comment: it does nothing in the program, and is only there for you to write notes to yourself.
The first two sections, Time-Related Constants and Simulation Constants, are just setting variables. It's like saying x = 3, so that later on you can do other operations with x.
The semicolon at the end of a line (in MATLAB) suppresses the output of the line. See what happens if you type x = 3; versus x = 3 at the command prompt.
In iteration constants, length is just a function that tells you the length of the vector.  X_rna_0 was previously initialized to go from 0 to 1.4 in steps of 0.2: the syntax is vector_name = start:step:end.
The simulation variables section is creating xyz-matrices, with all values initialized to zero.  The length in x is xr_max, and so on.  The idea is that, later on, at each step in Euler's method and each value of xr_max and xp_max, you'll save the value of X_rna.
The initial conditions are being set using meshgrid, which is best explained here.  The : means all of the rows/columns, corresponding to position: say you had a 3 x 3 matrix called apple.  apple[:,1]  gives you all the first column (1) of all three rows.  apple[1,:] gives you the first row (1) of all three columns. The .' means that the matrix is being transposed: again, the best way to see what's going on is to create a matrix of your own, perform the operation, and see if what you get is what you thought it would be.
For loops, you can read about here, for a start.  I do not think understanding this loop requires more information than that page.
Dot before ^2 means that each element of the matrix is being squared; you are not multiplying the matrix by itself.
That should decipher most of the code for you.  If you have further questions, feel free to comment here.
EDIT: Question 2 asks you to make a plot.  A plot of y vs. x would be made by typing plot(x,y)
Also, help on a particular MATLAB function can be accessed by typing help name_of_function.

This is a set of ordinary differential equations. Proceed like this

Make a matlab function for the ODEs that define the system (equations 1,2,3,4). The function should return a 4 dimensional vector which is basically the dy/dt (the rate equation)
in the main program declare the initial values of different components. There is no absolute rule for what it should be and it is based on your prior knowledge of the system
in the main program write a module to integrate the rate function over a time interval. there are several numerical algorithms to do it such as Euler, implicit euler, runge-kutta, polynomial interpolation- predictor corrector methods (Adam Bashworth) etc. If you want to improve your knowledge on the numerical methods then write your own code for any algorithm. A good book on basics of numerical methods can be referred. Otherwise, you can use inbuilt ODE solvers in Matlab.

A note on numerical methods for solving ODEs: what you precisely do is add-up and update the rate function in small intervals of time. The very basic method is euler in which you just implement this:
y = y + h*f(x,t)....... explicit/forward euler
y = y + h*f(x,t+h)...... implicit/backward euler

where dy/dx =f(x,t) and h is a small time interval
So what you have to do, exactly, is to run a loop which goes from t=t_initial to t=t_final with small increments of h. You can use any basic loop such as for loop or while loop. for loops are quite easy to implement. (the basic syntax is - for(initial;final condition; increment function) which in Matlab is as easy as for t=t_initial:h:t_final
Within the loop you apply the integration operation.
More advanced techniques use variable step size to improve the performance. You can use the inbuilt ODE solvers if you require better performance and accuracy.
As for your homework.. You already have the code; just need to put the parameters.


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I'd like to know the name and a few details of a certain time-keeping structure in the human brain
I once heard of this structure on the Discovery Science channel and have since forgotten the name. The details I remember about it were that it is the central time-keeping device for the brain located in the geographic center of the human brain. The DSC only mentioned it in passing to describe a person with an abnormality in this structure. Can someone post some reliable research links and a short description of it? I don't trust google much and am not good at using it, so thanks!

You are probably referring to the suprachiasmatic nucleus.
Note that, although this is the central clock, there are also so-called "peripheral clocks", for instance in the liver, pituitary and other organs that can finely tune rhythms in the organism.
You may also want to have a look at the Wikipedia page for circadian clock and references therein.

okay thank you very much, that looks like what i was referring to. I also heard it was very very small, and the wikipedia article said 20k neurons and the size of a grain of rice. I'll remember circadian clock too!

Suprachiasmatic Nucleus is a part of Hypothalamus, which might be an interesting read as well - hypothalamus is very important


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Why not use Cu(OH)2 as a dye for protein electrophoresis?
As I know, $Cu(OH)_2$ $+$ Protein $\rightarrow$ Purple. So why not use $Cu(OH)_2$ as dye in protein electrophoresis?

May be the OH-group changes the summational charge of the protein (which is very important for the separation), as by adding the compound, we change pH.
Still, copper is used in electrophoresis, but as CuCl2. http://www.ncbi.nlm.nih.gov/pubmed/2449094

Copper hydroxide does not dissolve very well in water, which means you will have trouble soaking them into your gels.
Also, even if you managed to add enough copper hydroxide beforehand (in the wells), it is unlikely that the copper(II) ions, if any existes, will travel along with the protein due to its size. (Copper hydroxide itself does not have any charge.)
As for the paper Stella mentioned, the copper salts are used after electrophoresis to produce a negative image, which is exactly what you cannot do with copper hydroxide.

Protein electrophoresis is often done in an alkaline pH (8.6), which is not exactly nice if you want to use $Cu(OH)_2$.
If you need quantitation, you can use Coumassie blue or Amido black. If you want sensitivity you can use silver. These existing stuff are quite OK.


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Should I design a primer to detect virus based on NCBI genebank?
When I searched HIV on NCBI gene bank, I found 2 results from 1997: http://www.ncbi.nlm.nih.gov/genome/?term=HIV. HIV can change every day, so I think the sequence from 1997 is not useful. Is it?

Please give some more information on what you are trying to do.

I'm trying to design a primer to detect HIV so i need an up to date sequence of HIV. But the one in NCBI Genebank is from 1997 and i think it's not useful anymore.

My impression from your questions is that you're doing DIY biology and are not in a corporate or academic lab. I'd very strongly suggest you to avoid doing anything with potentially HIV-infected material, handling this requires at least a biosafety level 2 laboratory. Handling HIV without proper precautions and permits could result in infecting yourself and potentially a lot of legal trouble or even criminal charges.

Hello, thank you so much for your advised. However, i just give an example. May be i will try on other virus/bacterial , should i using the sequence from NCBI to design primer when it's not up to date ? Any other database better than NCBI ?

@ĐứcUltraSoft you can look at highly conserved sequences in viral/bacterial genome. But as told in the other comment, don't work with pathogenic microbes.

@WYSIWYG If i have more result, like 1998, 1999, 2000 ... i can compare them and know which is the highly conserved sequences. However, how i know which is the highly conserved sequences when i have only 1 result from 1997 ?

you can.. certain regions of important viral genes such as reverse-transcriptase and Nef are conserved

@ĐứcUltraSoft Try searching Google Scholar or a similar engine for "conserved sequence HIV".

Any other database better than NCBI ?

A lot of people overlook some sub-databases inside NCBI and search the main nucleotide database only.
If You never tried it, you can blast the HIV sequence which You have found, against other databases. On the ncbi blast webpage, just choose the options other than nucleotide collection (nr/nt). I tend to find new sequences in Expressed sequence tags (EST), Genomic survey sequences (GSS) or Whole genome shotgun contigs (WGS). Some of these databases cover unfinished sequencing project and should be a source of new data.
(I am a plant person, not virus person, so maybe you will find out, that different databases are worth searching for you. Or you will find it a waste of time.)
BTW, now some time had passed since your question. How did you solve Your HIV sequence problem ?


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Some question about materials for PCR
I'm planning to order oligo, polymerase, nucleotide, buffer for my first diy PCR experiment (now I have nothing), so I have some questions.

How and how long I can storage them?  I have only a fridge that can freeze to -10 -> -20C.
I see the size/concentration of polymerase is 400 units and 25 nmole of oligo. So what can I do with 25 nmole oligo and 400 units of polymerase? How many PCR experiment I can do with 400 units of polymerase, and how many PCR experiment I can do with 25 nmole of oligo?
If I have a HPLC machine, can I reuse the polymerase by purify it after reaction?

At -20 C, you can keep things around for a pretty long time. I'm not sure that years is a good idea, but at least months.

The manufacturers of each component should have information available on their website regarding storage temperatures, along with recommended protocols on how much of each component to add to the PCR reaction. I would not try to reuse the polymerase, as depending on the kind you buy it may be a complex of proteins, and it may not be functional after purification. However, you're welcome to experiment all you want, it's your stuff!

1: -20 is the normal storage condition for PCR reagents in the lab so you should be ok. One warning: you should make sure that your freezer is NOT auto-defrosting. Most consumer freezers will cycle temperature to prevent frost build up. This is very bad for enzymes and will greatly reduce their lifespan. If you can’t find a non-defrosting freezer, you might be ok if you buffer the temperature by keeping your enzyme in a cooler in the freezer, or inside a block of metal with a hold drilled in it.
2: You can stretch your reagents by lowering the volume of each PCR reaction. 25uL is workable in the lab, but keep in mind that the smaller the volume the larger the relative error in your measurements becomes.
3: It seems strange to me that you have access to a HPLC machine but can’t afford to buy new enzyme when you run out. I really wouldn’t try to reuse anything. Maybe it could work, but would you really trust your results? If you shop around you can find cheaper brands of polymerase.

Good luck!

3: depends on the polymerase: some of the more expensive polymerases will loose some of their functionality (e.g.: "breaks" that avoid accidental polymerization prior initial heating)


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Can one die from pain?
Is it possible that a human or any other creature can die from pain?
I googled and found different answers. Some articles say Yes while others say No.

A related disease http://en.wikipedia.org/wiki/Fibromyalgia is not fatal.

This is probably very hard to study, since it will be difficult to disentangle pain and the reasons for pain (e.g. injury). However, I can imagine that extreme pain can lead to heart attack and death. In that case the direct cause of death would be heart attack but pain would be the underlying cause (probably along with other underlying risk factors). See e.g. http://www.nhlbi.nih.gov/health/health-topics/topics/heartattack/causes.html

@fileunderwater - Cause of death would be complications of shock, not pain. Can pain cause shock? absolutely.

Sure, f pain makes an organism not want to live, then I would consider it fatal. You can link it to satiety or whatever, diabetes put the body is a state outside of homeostasis. So does pain

I very much doubt it. You may however die from whatever's causing the pain. The reason you feel pain is so you stop doing whatever is causing the pain. Hence someone knows not to touch a hot fire because it is painful. But the pain itself is not actually the danger — it's the fire burning away skin. So pain is actually a good thing, a survival mechanism. So for something that is meant to prevent death it's hard to imagine it doing the opposite.
Perhaps if you were in SO much pain you may be unable to breathe and paralysed — but even then I still think you'd go unconscious before that would happen, and you'd start breathing again, etc.
The only other thing I can imagine is having a cardiac event, and the heart stopping. Again, this would be because of stress. Other than that — you may commit suicide on account of insufferable pain, however it's a different situation.
However pain never comes on its own for no reason, just like smoke needs a fire. In this case it's the fire, not the smoke, that will kill you!
People who've ever been in a desperate or life threatening situation like a car accident have often walked on a broken leg for example — feeling no pain. In this case the body was giving them a chance to escape what might have been a lion, etc.
In short, no, I don't think you can. However I cannot give a 100% correct answer. It would take just one example to prove that however!

One could imagine sending signals through the nociception system to cause pain perception without any actual physical danger to the body.

great answer! though the fire/smoke analogy is not so apt: "50–80% of fire deaths are the result of smoke inhalation injuries" http://en.wikipedia.org/wiki/Smoke_inhalation

Yeah, that's what I was saying - "in this case it's the fire that kills you". So it's essentially a reverse analogy, retrospectively I realise it was confusing!

Totally wrong answer, -1

"feeling no pain" because they're in shock.

The evolutionary functional answer here is probably not right. 'Expecting biology to behave a certain way is not a safe bet!'
Its a common misconception that all living things are designed to endure regardless of cost.  You can die from pain.  One can definitely die from fear.
This report tries to make a case though the diagnosis is not causal: Sudden, Unexpected Death in Chronic Pain Patients pretty much says it all.  "Unexpected, sudden death due to severe pain is poorly appreciated, since many observers still view severe pain as a harmless nuisance rather than a potential physiologic calamity."
It goes to further note the physiological stress of constant pain:
"Severe pain is a horrific stress. Severe pain flares, acute or chronic, cause the hypothalamic-pituitary-adrenal axis to produce glucocorticoids (cortisol, pregnenolone) and catecholamines (adrenalin and noradrenalin) in an effort to biologically contain the stress. Catecholamines have a direct, potent stimulation effect on the cardiovascular system and severe tachycardia and hypertension result Pulse rates may commonly rise to more than 100 beats per minute and even rise to more than 130 beats per minute. Blood pressure may reach more than 200 mmHg systolic and more than 120 mmHg diastolic."
Just to further the discussion of our evolved defiance of death.  I've long heard that rabbits can die from fright.  They don't put up much of a fight.  This is a typical experience with rabbit owners:
Rabbits Can Die of Fright!
It is possible for a rabbit to die of fright. Loud sounds, such as cats, dogs, loud music, or screaming can lead to a heart attack and put a rabbit into shock, causing sudden death. It can take several days for the rabbit to die this way, and it does not happen often, but it is quite possible.
And yes, People can die from fear too.

I refer the honorable gentlemen to James Harriet. He reports discovering by accident by ending the pain he was in some cases able to reverse the pathology by ending the pain with anesthetic drugs, thus allowing the body's natural healing abilities to take over.
He first discovered it in a sheep by accident (insufficient dose to put it down) and later used it effectively on dogs.


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Use of pigs for obtaining transplant organs
It is being said that organs can be obtained for transplant from the pigs. What is special about pigs that we are using them? Why can't we use monkeys or chimpanzees with whom we share a more recent common ancestor?

Here's the answer: http://en.wikipedia.org/wiki/Xenotransplantation#Potential_future_animal_organ_donors

Monkeys and many other primates are too small to provide organs that will provide the needs of a human host. The fact that primates are so close to humans physiologically is not always a win as transplanted organs will bring diseases into the host that can be quite dangerous.
Besides, because even human human transplants induce immune rejection of organs. Its typical that immune suppressants will be a lifetime treatment for the patient.
Finally, the cost of a pig organ is negligible and their organs are about the right size, and I would bet that activists don't protest pig transplants nearly as much as primate donors.


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Advantage of being deuterostome
We know that most of the so called "Advanced" organisms are deuterostomes (i.e., development of gut starts from anus). Is there any evolutionary advantage of that? If not, why and how did it evolve?

Your premise is quite doubtful. While you are considering vertebrates as the pinnacle of evolution, you should note that arthropodes, nematodes, annelids and mollusc, wich contain more than 95% of known animal species are, in fact, protostomes.

Are protostomes less complex/advanced than deuterostomes? Well, it is true that the sequenced genomes of the fruit flies and Anopheles Gambiae show that these genomes are slightly shorter than the one of the puffer fish or the human. Also, I would like to remind that correlation does not mean causality. Other traits that are associated with deuterstomia/protostomia are likely to explain the observed variance.

I think we have to go back even further.... I think the deuterostome and proteostome are a convergence of a body plans (development of body cavity) of two organism that diverged even earlier. It should be noted that all protostome have spiral cleavage at their 8 cell stage. While deuterostome have a radial cleavage. The cell fate of the blastosome of a protostome is determinate while in deuterostomes it is Indeterminate.


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Shade-loving Plants
In shade-loving plants, the light compensation point is reached at low irradiance because:
A. Leaves have more chlorophyll per reaction center
B. These plants have greatly reduced respiration rates
C. Shade-loving plants synthesize anthocyanins
I am mainly confused between A and C. I am sure that A is factually correct but I don't know whether it is correct in this context.

I think the answer is A. As for C, Anthocyanins are located in the vacuole and their light absorption does not affect the process of photosynthesis which occurs in the chloroplast. Anthocyanins do participate in prevention of High-Light Stress (or Photoinhibition) but they have no role to play in gathering light energy for photosynthesis. Therefore, to improve the quantum efficiency (quanta of light per CO₂ molecule fixed or O₂ evolved, or any other quantifiable photochemical event) of the light reaction, anthocyanins play no role.
But, if there are more chlorophyll molecules per reaction centre, i.e. there is a greater number of chlorophylls in the LHC (Light Harvesting Complex), or the Antennae system, then the quantum efficiency can be improved, the absorption band widened and thus the light compensation point is reached earlier. The extra molecules of chlorophyll  absorb energy at their specific wavelengths of light and transmit this energy to the main reaction centre by FRET(Fluorescence resonance energy transfer). Therefore, greater the number of chlorophylls per reaction centre, greater is the light energy absorbed and transmitted to the reaction centre and hence, better is the quantum efficiency.
More technically, having more chlorophylls open up more pathways for photochemical energy quenching, and thus improves the efficiency by minimizing fluorescent losses.


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Pathway mediates nitroglycerin-induced relief from angina pectoris
what kind of Pathway mediates nitroglycerin-induced relief from angina pectoris,please provide some idea...

This looks like a homework question. Can you please show what you have done so far to find an answer?

@Chris I missed my class so I really had no idea how to approach this question I did some literature search but it was confusing ..

The effect of nitroglycerin on the cardiac tissue is similar to nitric oxide (NO),  which forms in the endothelium of blood vessels from arginin metabolism products.
So, the general scheme can look like this:
R-NO2 is converted to R-NO outside of the cell (glutathion-SH-dependent reaction). NO is lipophilic and rapidly penetrates into the cell where it activates guanylate cyclase. From this moment you can see the resulting influence on myosin and actin on this picture:


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calculate the number of heterozygotes
The ability to taste PTC is due to a single dominant allele "T". You sampled 215 evolution students, and determined that 150 could detect the bitter taste of PTC and 65 could not. Assuming this trait is in Hardy-Weinberg equilibrium in this population and that there are only two alleles, calculate the number of heterozygotes for this trait there are in the population.

How do I formulate this into hardy-weinberg eqbm form need help.

This looks like homework. What have you tried so far?

Total  215  Calculations
Can taste PTC  150
Cam't taste PTC  65
For recessive  0.3023255814
Sqrt of recessive q  0.5498414148
p=1-q  0.4501585852
2pq  0.4950316667

Maybe just edit your question to add that information.

@krushna this site is not a homework answering service. I suggest you read this post about homework questions. http://meta.biology.stackexchange.com/questions/266/homework-policy-for-faq/267#267

Hardy-Weinberg law gives the frequencies of genotypes from allele frequencies: $p^2 + 2pq + q^2$
Because the allele "T" is dominant, the frequency you're directly measuring through the experiment is the addition of $p^2$ and $2pq$.
$$p^2 + 2pq = 150/215 ≈ 0.6976$$
solving for $p$ (and replacing $q$ by $1-p$) gives:
$$p = 1 - \sqrt{\frac{13}{42}} ≈ 0.45 $$
The frequency of heterozygotes is given by:
$$2p(1-p) ≈ 0.4950 $$
And the number of heterozygotes in a population of 215 individuals is given by:
$$215 \cdot 0.4950 = 106.43$$
That sounds very alike what you wrote in the comments!

yeah I calculated the heterozygotes frequency but I was clueless how to find the number...of heterozygotes...but thanks for your help..


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Why not produce protein based on condensation reaction?
I'm fairly new learning about protein. As I know protein can be synthesis by condensation reaction. And the current method to produce protein is purify them from an organism. So why not produce protein based on condensation reaction instead of purifying it from an organism?

can you give a link to the "condensation reaction"? I'm not sure what exactly you're referring to...

@MattDMo http://www.google.co.uk/search?q=protein+synthesis+condensation+reaction&bav=on.2,or.r_qf.&bvm=bv.49784469,d.aGc&biw=1366&bih=640&pdl=300&um=1&ie=UTF-8&hl=en&tbm=isch&source=og&sa=N&tab=wi&ei=XYjwUZmLIYSWiQeTpYHQBw

@ĐứcUltraSoft, because it is difficult to synthesize long proteins that way.. small peptides can be synthesized like that..

@WYSIWYG Thank you so much, now i understand.

The chemical synthesis of peptides has actually been used for a long time, see the Wikipedia entry or this schematic for some examples.

It is important to first remember that to do anything useful, the sequence of the amino acids in the protein must be exact. For example, sickle-cell anaemia is caused because one amino acid in a haemoglobin protein is incorrect. Because of this, peptide synthesis involves rather complex chemistry in order to ensure that amino acids are added in the correct order and number, and is only effect up to a chain of a few dozen amino acids.
Now it is possible to produce peptides of various lengths in a cell-free extract, which basically involves taking the cytosol out of cells (with all the ribosomes, tRNA's, and other factors therein) and adding the mRNA template to be translated and an ATP source. This way, a peptide can be prepared by using the cell's own machinery for protein synthesis without actually needing a viable cell.
Remember also that even if it were possible to chemically synthesize a correct peptide sequence, the protein would still need to fold into a correct 3-dimensional structure to work properly, which in some cases is impossible for any artificial method currently available.


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NaCl role in CTAB - DNA complex in DNA extraction
I have a question about the role of NaCl in the DNA extraction process. So for NaCl concentrations under 0.5M, CTAB and DNA molecules can create complexes.
In those concentrations, proteins and other hydrocarbons are still soluble in water except the DNA-CTAB complex. If we raise the concentration of NaCl then the complex of CTAB-DNA will be soluble to water too. Correct me if I'm wrong until now.
So I don't understand something. Why do we use NaCl?
Let's assume that we don't add NaCl. Will the CTAB create complex with DNA or not? As I read CTAB creates ionic bonds with DNA (phosphate groups). So in this situation (without NaCl) CTAB must be able to create complex with DNA too.
So why did we use NaCl? Just to keep proteins and other hydrocarbons soluble in the water or there is something else that NaCl helps in this complex creation?

CTAB forms insoluble complexes with nucleic acids and can be used to selectively precipitate them from solutions, see this reference:

The isolation of bacterial nucleic acids using cetyltrimethylammonium
bromide (Cetavlon)

When you add NaCl in a concentration between 0.4 - 0.7M, the nucleic acids stay in solution, while polysaccharides and other substances, which may interfere with the DNA preparation do not. See this paper: "Rapid isolation of high molecular weight plant DNA."


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Which was the last significant event in human evolution? What's next?
At 10.000 BC (12 ka), we became the last of the Homo species on Earth. In evolutionary terms this is a very little time range to something happen, but I'm wondering anyway, in this meantime which are the most significant changes in our species? Were there any?
Also, I've heard something about how our body hair and nails will be gone 'soon', there's any estimation of when such a thing could happen?!

The problem with most evolutionary changes is that they can mostly be seen only in review (except for developing a third arm probably). So we actually don't know what is going to happen next.

@Chris Sometimes we do know very well, but nobody listens.

@RodrigodeAzevedo What do you have in mind?

@Chris Intelligence. One generation is enough.

Background
I'd like to start by saying that phenotypic (loosely speaking phenotypic mean morphological) traits evolve because their variance in the population is correlated with some genetic variance. If most of the phenotypic variance is genetically coded, you'd expect that the trait will change through if different variant of the trait influence fitness (which is a function of both survival and reproductive success). Stated differently and more accurately the change in mean value of a given trait $R$ in the population is given by:
$$R=S\frac{V_{Ga}}{V_{P}} = S\frac{V_{Ga}}{V_{G}+V_{E}} =  S\frac{V_{Ga}}{V_{Ga} + V_{Gd}+V_{E}} $$
, where $S$ is the selection differential, $V_{G} = V_{Ga}+ V_{Gd}$ is the genetic variance where its two components are the additive and dominance genetic variance respectively. $V_P  = V_G + V_E$ is the phenotypic variance which two components are the genetic and environmental variances. The ratio $\frac{V_{Ga}}{V_{P}}$ has a name; it is called the heritability in the narrow sense symbolized by $h_N$ Note: I present here a simplified version of the reality!
So, if the trait you consider has genetic variance in the population and that this trait influence the fitness with a given selection differential you can provide estimates of how the trait will change through time in the human population. Now if the variance does not already exist in the population but you have to wait for mutations to occur, then you cannot really provide an estimate of when will this occur.
Discussion on the future evolution of nail size
Also, when you think about some traits such as our nails. You may consider that they are of no use but do you really think that those people that have no nail would really have a better fitness. At first I would tend to think that I would rather chose a partner that have nails, it is much more sexy! If many people are like me and appreciate nails, nailless people will have difficulties to reproduce or in other words, they will have a lower fitness that nailed people.
I don't think we have data on what loci (positions on the chromosomes) influence the size of the nails and about how much of the variance in nail size is explained by the genetic additive variance. And how do the size of our nails influence fitness. So we don't know about how this trait will evolve through time.
Future evolution of other traits
There are several traits that we can/could more or less predict their evolution. Those are the traits for which we know the ratio of the genetic additive variance over the phenotypic variance and how it influences fitness. I can think of genes that are linked with resistance to new diseases such as HIV for example. If malaria comes to a new area you might expect the allele (=variant of a gene) allowing a better resistance to malaria will increase in frequency (note that this allele is advantageous in heterozyotes (protects from malaria) but it is highly disadvantegous in homozygote because it causes sickle-cel disease). We could estimate the change in frequency of alleles linked with obesity in some countries also. Probably several studies exist on the subject but I don't know them. One might improve this answer by giving some information about how HIV resistant variants is likely to change in frequency through time.
What were the last evolutionary changes in human history?
You can think of the impressive frequency of the Tay-Sachs disease in french canadian due to a bottleneck effect. Or you may think of the evolution of height, about the evolution of the shape of the skull or the evolution of feet. You can think of the reduction of our gut. etc… Your question is not well enough define so that we know if you consider the raise in frequency of Tay-Sachs disease is sufficient for you to be called a significant evolution.
Hope that helps!

Yes, it helps... Thank you! By a significant evolution event I mean it in a more common sense way, like something that can be visibly noted on our anatomy and perhaps could have some comparative figures.

One example of an active selection pressure's effect on human phenotype is in areas where malaria is endemic, the prevalence of sickle cell anemia is higher.  Sickle cell anemia is highly protective against malaria, and less people die from sickle cell than die from malaria, so you see a rise of sickle cell in the population.  This is a small degree of phenotype selection compared to the sort of selective pressure that would be required to cause the degree of evolution you are talking about, but it's one of the few things that can be readily seen in the modern world.  Most people in the modern world live long enough to reproduce, and survival of the fittest has less influence on us than it did in our tribal days.
To wax philosophical, one might argue that the media (e.g. Hollywood) has exerted a selective pressure over our evolution, as it has significant influence over what people deem "beautiful" and "attractive," thereby altering our ultimate mating selection behaviors.


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Troubleshooting for Agarose Gel Electrophoresis
SI ran my 2% agarose gel on constant voltage (100 V). For a few times it worked at CV but, after a week or so the machine would automatically switch to constant current by itself. And this only happens when I try to increase the voltage to 100 V. It works fine between 50-80 V. Beyond 80 V it keeps fluctuating between CV and CC.
Is there a problem in my power supply (GENEI electrophoresis power supply) or is the TE buffer that I am using? Although I checked its pH and it's fine.

Can you provide a few more details (you can edit your post to do so): At what voltage do you run you gels? How big are they? Which powersupply are you using?

I haven't found a manual for this machine, but my guess is that you exceed the maximum current which the power supply can provide. This is something I have experienced myself for electrophoresis.
Usually power supplies then switch into the constant current mode at the maximum current they can deliver, which I think is what happens here. If the voltage you choose is lower, you do not run into this limitation, thats why it is working without problems.
So you can either run your gels at constant current, which makes them run faster but also produces more heat, which can make your gel blurry. Or you live with a slightly smaller constant voltage, have your gels run a bit slower, but probably have a bit better resolution. I have to say that I have never had any problems with the resolution, even when I ran my gels really fast.

alright great. these days i'm sticking to a lower voltage itself so i'm not facing any problems. but i just wanted to know the reason why. thanks guys it makes sense now :)

Gel melt can cause relly problems with low melting agarose. I have seen this at a colleagues gel once....


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Body's response to second dengue attack
I have read in wikipedia that the first dengue virus infection is cleared by the body very easily. The second infection, however, is dangerous. How does body fight second infection, or does it has any tool to fight it given earlier antibody will be ineffective?


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Do IgM and IgG differ for different infections?
I am not that much educated in the medicine and immunology fields. So I noticed that there are tests for IgM and IgG immunoglobulins for various infections. I was not able to google quickly if IgM for one type of infection differs from the one for another type of infection.
I guess they differ because otherwise there would be only a few tests in the laboratory instead of dozens. But it would be great to hear some solid explanation.

IgM (Immunoglobulin M) is the first antibody to appear in response to an antigen. It can be produced by the fetus and cannot be crossed by the placenta.
Typically one might test IgM to diagnose hereditary and acquired IgM immunodeficiencies or diagnose Waldenstrom macroglobulinemia. It can serve as the earliest Ig serologic diagnosis of infectious disease.
Lab tests for IgM may be increased in liver disease, chronic infection, hyper IgM syndrome, and secondary to nephritic syndrome; Waldenstrom macroglobulinemia, lymphoma, CLL, multiple myeloma (rare), Schnitzler syndrome, cold IgM antibody agglutin, and MGUS.
Lab tests for IgM may be decreased in protein-losing syndromes, non-IgM myeloma, and infancy/early childhood.
IgG (Immunoglobulin G) activates complement and fights infection. IgG represents 70-80% of the total serum immunoglobulins in normal adults. It exists in four subclasses (IgG1, IgG2, IgG3, and IgG4). IgG1 predominates as 65% of the total IgG. IgG of maternal origin provides passive immunity to the neonate. It is transported across the placenta.
Typically one might test IgG to diagnose IgG myeloma, diagnose hereditary and acquired IgG immunodeficiencies, and provide a serologic diagnosis of infectious diseases and immunity.
Lab tests for IgG may be increased in multiple myeloma, solitary plasmacytoma, MGUS, lymphoma, CLL, sarcoidosis, cirrhosis, autoimmune diseases, parasitic diseases, chronic infection, and intrauterine contraceptive diseases.
Lab tests for IgG may be decreased in protein-losing syndromes, pregnancy, non-IgG myeloma, Waldenstrom macroglobulinemia, primary immunodeficiency states, and agammaglobulinemia (if combined with other immunoglobulin decreases).
Sources:
https://5minuteconsult.com/collectioncontent/2-152356/lab-tests/immunoglobulin-m-igm
https://5minuteconsult.com/collectioncontent/2-152354/lab-tests/immunoglobulin-g-igg

Taylor, thank you for your answer that's all wonderful. But it actually does not address my question. I was asking why there is an IgM test for e.g. Borrelia burgdorferi and also the IgM test let's say for tick-borne encephalitis and they are priced differently.
In other words I was asking how exactly the IgM for one infection differs from the IgM for another infection.

IgM will be specific for certain epitope on the antigen. Basically, it will detect a "signature" of the various pathogens and be specific for it. Most of the IgM molecule will the be the same apart from a section called the hypervariable region. This hypervariable region will have different characteristics and specificity for each antigen that an organism has been challenged by.

Joseph, thanks a lot. Could you put this comment as an answer and I will accept it.

The CDC currently recommends a two-step process when testing blood for evidence of antibodies against the Lyme disease bacteria. CDC
If Lyme Disease is suspected in at-risk patients, a sensitive serum serology screening test is performed to detect IgG and/or IgM antibodies to Borrelia Bugdorgeri. More specifically, an ELISA (Enzyme Linked Immunosorbent Assay) is a type of test that is used to detect IgM and IgG B. Burgdorgeri antibodies which is then followed by a Western blot test.
In tick-borne Encephalitis (TBE), laboratory diagnosis depends on the detection of specific IgM in either blood or CSF (Cerebral Spinal Fluid), which usually appears later, during the second phase of the disease. CDC
Pricing is dependent on the number of tests required to accurately diagnose one or both conditions, associated laboratory fees, your medical insurance coverage, etc.

You are very welcome Alexander. Glad I could provide some clarity.

My mistake, sorry for that.


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What is this spider from Arizona?

I live in Phoenix, Arizona, USA. Can you please identify this spider for me. Is it dangerous?

It's hard to judge from a single photo but it appears to be from the Family Theridiidae (cobweb spiders). Spiders in this family have long front (first legs)and much shorter third legs as the spider in your photo seems to have. But the perspective may be off. You don't mention the size which would help.
I enjoy photographing insects and spiders in my area. One thing I found when I was trying to identify spiders is colour and pattern can vary quite a bit from different locale. Sometimes two spiders of the same species could look like two completely different species.
So please bear this in mind. All I am is an arthropod enthusiast that has benefited from some more skilled and knowledgeable people helping me out. With that in mind, I wonder if your spider might be Phylloneta pictipes (syn. Theridion pictipes).

Source: http://bugguide.net/node/view/2209
I should've said but the two spiders above are the same species; male on the right and female on the left.
You can check out more spiders of this species at http://bugguide.net/node/view/49080/bgimage and see how they vary.

The spider is a spotted orbweaver (genus Neoscona)

Probably of the species: Western Spotted Orbweaver (Neoscona oaxacensis)
This photo I attach came from a gallery of western spotted orbweaver observations filtered on only observations from Arizona:
https://inaturalist.ca/taxa/123713-Neoscona-oaxacensis/browse_photos?quality_grade=any&place_id=40


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Why do cartilaginous fishes not excrete ammonia?
My teacher taught me that bony fishes are ammonotelic while the cartilaginous fishes are ureotelic, but why does that happen? Why do cartilaginous fishes not excrete ammonia?

This is an interesting question. Most fish are ammonotelic, meaning the excrete ammonia (which is toxic to vertebrates) through their gills, which is a very energy efficient way (reference 1 and 2).
However some fish cannot go this route. If fish live in a very alkalic environment, excretion of ammonium ions is not possible. These fish have to convert ammonia to urea which is subsequently excreted (reference 3).
Most fish who are ureotelic use this as a strategy to control their osmotic balance. This means they keep their blood slightly hyperosmolaric compared to the surrounding sea water to prevent them from dehydration in the water and to regulate their body fluids.
This is achieved by a mechanism called "urea retention" and is an almost complete reabsorption of urea in the kidney of these fishes. Urea is then used in the plasma to maintain the high osmolarity there (reference 4 and 5).
This process also helps maintaining water for the animals but comes at a cost: The amount of energy used for osmotic regulation varies between species, but it is estimated to be around 10-15% of their standard metabolism, which is also a reason why a lot of fish directly excrete ammonia (reference 6).
Excess urea is ultimately excreted through the gills of the fish.
References

The multifunctional gut of fish
Ammonia Production, Excretion, Toxicity, and Defense in Fish: A
Review
Urea excretion as a strategy for survival in a fish living in a very
alkaline environment
Morphological and functional characteristics of the kidney of
cartilaginous fishes: with special reference to urea reabsorption
Living with high concentrations of urea: They can!
The Energetics of Osmotic Regulation in Ureotelic and Hypoosmotic
Fishes

But why cartilaginous fish? Are they more likely to live in an alkalic environment?


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Skull size of Homo naledi
I want to 3D print the skull of the newly discovered Homo naledi.
The printing data can be found here: http://morphosource.org/index.php/Detail/MediaDetail/Show/media_id/7300
Where can I find the exact size of the skull so that I get a 1:1 copy? Google was of no help.

@Tusky: I think this would be helpful!

From the link:a cranial volume of 560 cm3 (34 cu in) for the males and 465 cm3 (28.4 cu in) for females, approximately half the volume of modern human skulls; average Homo erectus skulls are 900 cm3 (55 cu in). You could use these data?

Based on Figure 11 in the original publication (scale bar = 10 cm):

The anteroposterior length of the skull should be about 16.3 cm. I just printed out the figure and did the conversion.
So check that your 3D printing software estimates a little over 16 cm for the length from brow ridge to occipital. The full reconstructed skull will be longer of course, but this should give you a concrete measurement to compare to.

Yowza! That's quite the brow! Guess no hats for H. naledi!


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Why males are more prone to cardiovascular diseases such as heart attacks than females?
I often see more people of males undergoing treatment for heart disease. It is often said that female reproductive hormone (oestrogen) has some cardio-protective action by preventing constriction of coronary arteries. Can any one explain this?

Can you please provide some reference to support the statement? Your observations can be biased and the sample size may be too small to make such claims.

A potential cause is the different distributions of body fat in males and females.
Men typically store their fat in their midsections and women store it in their hips/legs.
Ectopic fat, a type that puts people at a greater risk of cardiovascular disease, is stored more in the midsection of people.
Therefore, men are more likely to get cardiovascular diseases.
https://press.rsna.org/timssnet/media/pressreleases/14_pr_target.cfm?ID=1983


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Can you identify the species?
Sighted today. Its feathery tail was moving.

Please see https://biology.stackexchange.com/tags/species-identification/info and edit your question.

Using your link and a basic Google search using your descriptive words "moth with feathery tail", similar images were found.  It appears to be a female moth of the genus Diaphania.  There appears to be many species in this moth genus, and several look similar. Assuming you live in North America, it is probably Diaphania hyalinata. It is most commonly called "melonworm moth" and looks exactly like your linked image. Apparently they can do garden damage and can be considered a garden pest. That was good coffee.
https://en.wikipedia.org/wiki/Diaphania
https://bugguide.net/node/view/237001/bgimage
https://bugguide.net/node/view/7924/bgpage
http://www.growingproduce.com/vegetables/pest-of-the-month-melonworm-2/


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What are the various types of protein-protein interactions
I understand there are a number of protein-protein interactions, but what types of interactions exist? and what are the characteristics of them?

Characteristics? They happen between proteins.

characteristics of the interaction type, i.e, what makes a hydrophobic interaction?

I would suggest asking "what are the various types of protein-protein interactions"

There are so many types of protein-protein interactions via various domains, such as SH2 binding (in RTK signaling), Pleckstrin Homology domain (involved in signaling) among others. This site gives a nice list: http://pawsonlab.mshri.on.ca/index.php?option=com_content&task=view&id=30&Itemid=63
Of course, protein-protein interactions rely on the premises of basic biochemistry:

van-der waals interactions (at the most basic level)
Electrostatic interactions
"Lock and Key" model: Some proteins have specific binding pockets for domains of other proteins
Induced fit

There are many ways to study protein-protein interactions, including, but not limited to

Pull-down assays
2D SDS-PAGE / MS
Yeast two-hybrid
Immunoprecipitation

jp has a good point - technically there is no 'hydrophobic force' but when computations are done, a hydrophobic term is often made in the calculations.

Although hydrophobicity isn't a "force", shouldn't it still be included in the answer (creates an entropic advantage)?


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Basic Amino Acid Residue Binding Mechanism to DNA
I understand that many protein DNA binding domains bind to DNA via basic residues such as Arginine and Lysine. But what is the mechanism used to bind to DNA and where on the DNA would these residues bind?

This question has no particular answer.  There are several families of DNA binding proteins, some of them bind specifically (e.g. restriction enzymes like EcoRI which binds to and cuts GAATTC or transcription factors like lac repressor which binds a particular point of the e coli genome about 25 base pairs long) and some of them bind semi-specifically (e.g. zinc fingers which bind GC rich regions), others non specifically (e.g. the sliding DNA clamp).
For all of these proteins, they will have a tendency to have positively charged amino acids facing the DNA because the DNA's phosphate backbone is negatively charged.  There are lots of protein motifs (like the helix turn helix motif) that fits into the major or minor groove of the DNA.  The lysine and argenine are important because they are the positively charged amino acids.  Histidine is also positively charged, but it is not as long and flexible, and doesn't seem to fit as often or as well.
http://en.wikipedia.org/wiki/DNA-binding_protein

I'd make a comment if I could, but our lab has worked with a lot of poly lysine peptides for binding DNA. In our experience, lysine works better than arginine, and both work a lot better than histidine. Histidine has a lower pka, so it tends to be less positively charged at physiological pH. As far as proteins binding to specific DNA sequence, the double helix has two grooves, major and minor. The "sides" of the base pairs are accessible through the grooves, and proteins probably recognize patterns in those grooves. An A-T pair presents a different shape than a G-C pair, and DNA binding portions of proteins can discriminate these bumps and bind to the helix.


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Protein Biology Cheat Sheet
I'm looking find a cheat sheet for protein biology to stick on my desk to remind of some of the key principles of protein biology. I seem to remember the specific and complex principles in protein biology but at the expense of the basics.
Can anyone point me to a protein biology cheat sheet or formulate some suggestions to go on one?

EDIT
What I am looking for:

Amount of amino acids in a helix turn
Amino acids typically found in Beta sheets and Helices
The types of protein interactions (i.e. ionic, hydrophobic) and the  amino acids usually involved.
Definition of Globular and fibrous form
Types of post-translational modifications
Any other useful characteristics

Related: a friend of mine created this periodic table of aminoacids. The original is in Italian, but an English translation is attached at the end of that forum post. Also, svg sources are available and it is under a BY-NC-SA CC license so you can modify/expand it to your liking.

I think this is a question about what else should be on a protein cheat sheet.
If you are clever you can format this to have a very high density of information. A good project.
Here's my list - I never made a sheet though.  Also I tend to be interested in protein structure, so there's a bias here.

The frequency of the amino acids in say e coli or the PDB
The average molecular weight of an amino acid (~110 daltons)
avg backbone width of a sheet (5 x 6 Ang) and helix (12 Ang.) DNAMajor groove is also 12 Ang btw.
common non standard amino acids (ornithine, seleneomet, etc).
common post translational modifications (e.g. T/Y phosphorylation)
common non standard secondary structure (3-10 helix etc) or a small ramachandran diagram
pKas of amino acids - remember that charge is defined at pH 7
the genetic code

For alpha/beta propensities, I would use chou-fasman's numbers.  Its annoying because there are some amino acids in both lists.
I will try to think of more and add later...

You can find the answer in any university-level biochemistry textbook.
I would recommend you Lehninger Principles of Biochemistry, if you could find it in your university library.
Skim the list of content, find corresponding chapters and write it down. It won't take you several hours.


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How was the guided daily amount (GDA) calculated?
We are constantly shown nutritional information on food packaging stating this food contains "x" amount of your guided daily amount. A linked to the values is here. How were these values calculated? How do we know that men as a recommendation must not consume more than 2500 calories, 55g of protein 300g of carbohydrate etc...

Many of those values are unfortunately probably made up, or at least meaningless due to the extreme variance in populations.

So not even an educated guess?

Probably an educated guess, I'm sure they funded it on some research... but it was probably not an excessive effort. They knew just as well as everyone that humans vary too much to postulate a general amount of nutrients everyone needs, so it was more important to get exactly what it is - a guideline.

The total calories are not in fact a recommended value - they are an example amount that is derived from some calorie intake that seemed reasonable to someone (I don't know the details). It does not mean that the government is recommending that you eat exactly 2000 calories per day.
The relative content is, however, a recommended value, based on presumably research. So, if you do take 2000 calories a day, then you know how much of it should be fat/carbs/proteins.
I think that there is some controversy about whether the recommended values were influenced by industry lobbying. Moreover, science is definitely not clear on what the optimal food content for a human is, which is why we keep having the different diet fads, oscillating from no-fat to no-carbs.

In the USA, they refer to this as the recommended daily values (DVs) for a variety of nutrients. All I can find regarding these recommendations is that they were calculated for adults and children over 4 years old with a daily energy intake of 2000 kilocalories (often referred to as calories in the US).


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Mechanism of syndesmophyte growth in AS
Ankylosing Spondylitis (AS) causes inflammation around joints and the growth of syndesmophytes that may eventually fuse vertebrae. I'm familiar with the genetics (HLA-B27, IL1A) related to the condition, but I can't find any information about the mechanism that causes the actual growths to occur.
My current assumption is that AS causes the over-production or under-production of a particular compound or enzyme at the growth site, but I can't find any studies or papers that explain this. Is the mechanism known? Is it directly related to abnormal levels of a particular substance?

As far as I remember the pathology course from medical school, chronic long-lasting inflammation often leads to proliferation of connective tussie and ultimately to fibrosis.
The actual mechanism here is the lack of oxygen which is used-up by different immune system cells to produce peroxydes and superoxydes.

Interesting. So the symptomatic inflammation over long periods of time ultimately causes fibrosis and fuses the vertebrae? Also, what causes the lack of oxygen at the site?

Not only symptomatoc, any inflammation (including the idiopatic one) would do. There are many reasons for hypoxie here: decreased blood flow rate, swelling etc.