text:
How can both strands of DNA code for proteins with similar functions?
It's not clear from the question but for example:
AAAAAAA
TTTTTTT
The top strand would create a different protein than the bottom, and with the huge amount of nucleotide in a gene, I think it's very unlikely that the same region on both gene could create proteins that are similar to each other, even though they're alleles of the same gene. This would also affect codominance/incomplete dominance, since I'm assuming that only one of the strand would create a functional protein.

Welcome to SE-Biology. However I'm not clear what you are asking. The use of 'can' in your question suggests that you think that this happens, in which case your assumption is wrong. The actual question suggests that you are asking a hypothetical question (in which case you should change 'can' to 'could').  However as you go on to say that in this hypothetical case you assume only one strand would create a functional protein, this seems less of a question and more thinking aloud. Please clarify.

Is this a duplicate of this?

You are confusing the the forward and reverse strands of DNA as two alleles. They are not. Remember you have a double stranded DNA from each parent. Each of those two pieces of double stranded DNA represent alleles for a given locus.
For the example you gave, you can have different genes that overlap the same region of DNA. One is on one strand and a different gene is on the other. The DNA is read 5' to 3' so we think of one strand as forward and one strand as reverse.
See embedded pic for examples from this publication about different kinds of overlap and whether they are conserved across species.

But the poster is asking about proteins, and not all those genes pictured are protein coding.

The figure shows both protein coding and non-protein coding. I addressed the misunderstanding of alleles, which seemed to be the reason for the confusion on how two "alleles" could produce a protein what was supposed to be very similar.  This stemmed from a misunderstanding of coding/template strands for a given allele vs. two separate alleles. At least that was my interpretation.

In general, protein-coding genes don't overlap, so the problem you've identified doesn't come up.
And no, complementary strands are not different alleles.  If that were so, bacteria and gametes would have two alleles of every gene, because they each contain one double stranded copy of the genome.
You have two copies of each double-stranded chromosome, that is why you have two alleles for each gene.

I think it's very unlikely that the same region on both gene could
  create proteins that are similar to each other, even though they're
  alleles of the same gene

I think your reasoning is faulty here. It's not that the two alleles are in the same chromosome and each in one strand. Each allele is in a different chromosome (one from each parent).
Overlapping or nested genes are a different topic altogether.

So brown eye allele is at the 5' end of the maternal DNA, which means the paternal's green eye allele is at the other 5' end, so that they're at opposite ends?

I made a diagram since perhaps it's the easiest way: https://s21.postimg.org/kap5b2gsn/Untitled.png

Usually not the whole gene overlaps, and it's not usually in-frame, this makes it a lot easier.
You also have some flexibility because of the redundant codons (20 AA for 64 codons), so you can more or less change every 3rd base to fit the "other" gene.
"Similar" could mean anything, possibly referring to two proteins that are not even 20% identical. At 20% identity you can still be sure that that enzyme is of the same class, catalyzing the same reaction. It might accept different substrates, but it could also still accept the same substrates.
Together, this means that on the non-coding strand of every gene you can put a gene coding for a protein that's more or less doing the same thing.


text:
Are all 23 chromosomes connected as one long strand of DNA?
This has perpetually confused me. Is our genome made up of two long strands, each strand made up of 23 continuous chromosomes that bind together, or are they 23 free floating separate pair of chromosomes? I think it's the latter because I just learn that genes on different chromosomes assort independently, which would be hard if the genome was a long string, but I'm still not sure.

According to what I've learnt, we have 23 independent pairs of chromosomes. Each of them contains 2 chromosomes and different kinds of genes. The genes are connected in one strand. So it is the latter one. And the 23rd pair of chromosome is used to determine our gender actually. Females got XX and males got XY

Not quite. Humans have 23 pair of chromosomes. That means 46 independent entities. Except for guys, we're one short.

@bpedit Actually, males have 46 chromosomes as well. The 23rd pair is X and Y. While the Y chromosome is much smaller than the X, it is still a full chromosome. Not sure where you got the "we're one short" idea...

@MattDMo Ouch! You're correct. Am deleting comment. Suspect this is age related.

DNA does not run from one chromosome into another.

I think it's the latter because I just learn that genes on different
  chromosomes assort independently, which would be hard if the genome
  was a long string, but I'm still not sure.

Though chromosomes are NOT connected by DNA, your gene access argument is, furthermore, not a great argument. It would just be one tiny strand of DNA between two very-much larger chromosomes. The nucleus is able to operate with much tighter/difficult problems with respect to accessing DNA.
I'm glad you're thinking of it physically though ! Chromosomes are indeed kept track of and connected by nuclear-cytoskeletal stuff.

Since both of these answers are downvoted, and the downvoter provided no feedback on what is incorrect--can someone comment to teach me and the community what's correct/incorrect?

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Altruism in viscous (asexual) populations
The viscosity of a population is the tendency of offspring to remain
near their place of birth. Taylor 1992 ("Altruism in viscous populations") provides a model to study how viscosity affects the evolution of altruism in a patch-structured population. In Taylor's model, the marginal inclusive fitness is given by
\begin{equation}
  W = bR -c - s^{2}(b-c)R
\end{equation}
where $R$ is the relatedness of a mother to random offspring born on her breeding patch and $s$ is the probability the offspring will remain on the natal patch. The altruistic act creates $b$ offspring with average relatedness $R$ and $-c$ offspring with relatedness 1.
My question is about the term $s^{2}(b-c)R$. Taylor explains this term as follows:

these b - c extra offspring remain on the natal patch with probability
  s and will therefore displace s(b - c) random individuals competing
  for the next generation breeding spots on that patch, and these will
  be native to that patch with probability s and in this case will have
  average relatedness R to the actor. Thus these displaced individuals
  will have average relatedness sR (p. 353)

My question is: Why is the average relatedness $sR$ (as opposed to $R$)? In other words, why is the term that accounts for competition among relatives $s^2(b-c)R$---as opposed to $s(b-c)R$?

The $sR$ that your looking at is the average relatedness of the next generation.  This assumes that the new immigrants into the the population are completely unrelated. So if the population is completely viscous ($s=1$) the average relatedness of the next generation equals that of the current generation.  On the other hand, if the population is not viscous ($s=0$) the next generation would be entirely unrelated because it would only be made up of unrelated immigrants.
The $s(b-c)$ is the number if individuals that are displaced by new offspring.  Again if all of the new generation sticks around ($s=1$) then the number of displaced individuals equals the number of new individuals.  And if all new progeny leave ($s=0$), there are no displaced individuals.

Thanks for your answer @Adam C. Now I understand that the relatedness after migration has to be a fraction of $R$. But why $sR$ exactly and not, say, $s^2R$ or any other fraction of $R$?

It is specifically $s$ and not some fraction or multiple of $s$ because the model assumes all incoming migrants are entirely unrelated ($R=0$).
For example, if $s=0.5$ and $R=1$, half of the population leaves and is replaced by incoming migrants in the next generation and all that remain are perfectly related.  So, in the following generation, 50% of population has an average relatedness of $R=1$ (those that stayed) and 50% of population has an average relatedness of $R=0$ (those that just arrived). Therefore the average relatedness for the entire population is $sR$ or $0.5$.

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text:
Discrete vs Continuous Replicator Dynamics
The replicator eqn in the case of discrete non-overlapping generations and asexual reproduction is given by the discrete replicator eqn:
$$x_i(t+1) = x_i (t)\frac{f_i(t)}{\bar f (t)}$$
where $x_i$ is the frequency of the strategy $i$ and each individual playing strategy $i$ produces $f_i$ copies of itself in the next generation. $\bar f$ is the average fitness. Thus
\begin{equation}
\Delta x_i = x_i(t) \frac{(f_i(t) - \bar f (t))}{\bar f (t)}
\end{equation}
In the case in which $x_i$ is a continuous variable, we have the continuous replicator eqn given by
$$\dot x_i = x_i (f_i - \bar f)$$
Question: I suppose we should be able to derive the continuous replicator eqn from the discrete replicator eqn by evaluating the discrete replicator eqn for $\lim_{\Delta t \to 0}$. How can I do this derivation?

To make this derivation, it is better to focus on the population size of a strategy as opposed to the frequency of a strategy. Let $N_i$ be the population size of the strategy $i$. Strategies in the replicator dynamics change exponentially. The equation for continuous exponential growth is $\dot N_i = f_i N_i$. Since $x_i=N_i/N$ and $\dot N = \bar f N$, calculating $\dot x_i$ by using the quotient rule gives us the continuous replicator eqn.


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How does a "chromogenic mixture" produce such pronounced color differences in this Agar Art?
The Forbes.com article Bacteria Become Art Tools In Annual Agar Art Competition says:

...People’s choice winner Zita Pöstényi, a microbiologist at SYNLAB Hungary Ltd, used three agar plates and four different bacteria to create a pattern inspired by Hungarian folk art.
[...]
Pöstényi used another trick to create her colorful plates. “I used a special media for this drawing,” she says,  “It contains a chromogenic mixture which enables the detection of activities of specific enzymes.” Thanks to this special mixture, the four bacteria species she used all showed up in different colors, which allowed her to create the traditional folk art pattern.
Usually, these unique colors tells researchers something interesting about the bacteria, but for the ASM Agar Art competition, these colorful features have become the medium.

Question: How does a "chromogenic mixture" result in different bacteria showing up in different colors in such a vivid way?

American Society for Microbiology Agar Art 2019 Contest, People's Choice. "Hungarian Folk Art," Zita ... [+]ASM / ZITA PÖSTÉNYI

She is referring to a mixture of chromogenic substrates: molecules which are more or less colourless until cleaved by a specific enzyme, releasing a coloured product.
For example X-gal is colourless until the enzyme beta-galactosidase hydrolyzes it, releasing a blue coloured product. If you spread a mixture of bacteria onto a plate, with some expressing beta-galactosidase and some not, you will see both blue and colourless colonies, as seen here:

[source]
Chromogenic substrates are often used to create differential media that allow the differentiation of different species of bacteria. This plate, for example, contains several different chromogenic substrates (a mixture, if you will) for identifying the bacteria commonly found in urinary tract infections:

[source]
If you wanted to make a picture with this plate, you could “paint” with Enterobacter spp. for blue, Staphylococcus aureus for yellow and S. saprophyticus for pink. Each species produces a specific enzyme that acts on a specific chromogenic substrate in the plate, changing its colour.
Alternatively, you could express the desired enzymes recombinantly in one species.

Thanks for the authoritative, well-sourced and colorful answer! With a CMY mixture and bacteria with variable expression rates of three enzymes one could make quite a palate.

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text:
The ring formation of ringworm
I know ringworm is caused by a fungus on the skin, nails or scalp but what causes the rash to form as a ring instead of like a normal spread out rash?

Maybe the fungal spore infects 1 point in the skin, and the hyphae spread out through the skin in a circular pattern. The ring would be where the edge of the hyphae is.

dermatophyte fungi
Ringworm is caused by a several species of Trichophyton fungi (T. rubrum, T. tonsurans, T. interdigitale, and/or T. mentagrophytes); and a couple others are well known (Microsporum canis, and Epidermophyton floccosum).
The ring pattern is not unique to ringworm causing fungi. (Fairy) Rings are totally common with fungi because mycelium grows outward from the center; and as the mycelium grows, the inner mycelium often dies (from starvation, age, attack by immune system?, or it is cannibalized) leaving only the outer ring of mycelium, which may continue expanding.

Unfortunately the medical world doesn't spend much time on the problems that they can already solve (like with an antifungal ointment or pill), so there hasn't been much effort devoted (to my knowledge) toward answering the mechanistic questions of ring formation of dermatophytic fungi. But it is known that some Trichophyton species sexually reproduce and Trichophyton rubrum also probably does reproduce sexually (ie., plasmogamy, karyogamy, and gametangia). I don't have any grounds for mentioning it (besides logic), but sexual reproduction is probably "age" related in fungi as is growth- so, a ring may be more pronounced in an area where fungal hyphae conjugate... much like the expression of fruiting bodies of other mushrooms.

Hmm.. I too find the question interesting and the fairy rings came to my mind. The dermatophytes are keratophilic and feed on keratin. Fairy rings spread circular coz the centre is now devoid of nutrients. It is ok to relate that way but the host immune reaction should not be left unconsidered... There must be some references hidden deep in litereature :) Hope someone digs it out!

the fairy ring phenomenon may not be a good analogy. Apart from host responses, nutrients are unlikely to run out on the skin which constantly makes keratin that dermatophytes live on.
Incidentally, there are a number of infective and non-infective conditions which have a ring-like or annular morphology. Lupus vulgaris, a type of tuberculosis, mid-borderline leprosy, pityriasis rosea,  granuloma annulare and erythema annulare centrifugum, idiopathic inflammatory disorders and annular variants of lichen planus and psoriasis are some of them. So there must be more to it


text:
Incubation time of Antarctic Phosphatase in lab
Antarctic Phosphatase is used to catalyze the removal of 5' phosphate from DNA. If I'm using it in the lab on a sample of 1-5 micrograms of digested DNA, how would I figure out how long to incubate the sample at 37 degrees Celsius?

I typically just react it for an hour, that amount of DNA doesn't seem excessive.

This set of protocols was really helpful for me when I got started cloning.

VTC because not looking up the manufacturer protocol counts in my opinion as an unresearched homework question.

For 5' extensions or blunt ends, incubate the sample for 15 minutes at 37 degrees Celsius.
For 3' extensions, incubate the sample for an hour.
https://www.neb.com/protocols/1/01/01/vector-dephosphorylation-protocol

Depends on amount of enzyme added.


text:
What software/approach to use to build a graph based on microarray gene expression correlation?
What software to use to build a graph based on microarray gene expression mutual correlation?
I have tried Cytoscape`s Reactome FI and a recipe from R bioinformatics cookbook, however, need a more reliable robust software or R/Python tutorial on how to make a graph with gene-nodes and edges built on the rule of significant (p<0,05) positive and negative Pearson/Spearman correlations.

do you have any examples of similar graphs - perhaps an illustrative example could help (draw one in powerpoint and save it as an image) plus some idea of the data, and what you are trying to show

I'm voting to close this question as off-topic because this is not related to biology but is basically about how to visualize a graph/network. How to build gene networks from expression data is still a valid question but that is not what is asked.

Hi @VassiaAlk - Cytoscape is pretty well designed for constructing a "network" of genes that are connected by their degree of correlation in expression; check out the online resources (e.g. http://apps.cytoscape.org/apps/expressioncorrelation). This site is aimed at biological questions, therefore this is off topic. Best


text:
Whole genome sequence analysis software
Please help to choose Bioconductor R packages and other software for the whole genome sequence data analysis and, in particlular, the goals of false discovery mutation rate, mutations exclusion, mutation contribution and data dimensionality reduction. I could find Expander, MeV, Genesis software for the microarray experiments, however, could not find similar tools for the whole genome sequence analysis of mycobacteria. Sorry, that my question has no code.

What is your question?

This is a good question! why is this getting close votes? it is slightly incoherent and badly written but it definitely merits a response!

Have you searched biostars.org?  That is a bioinformatics board, and I'd say about half the content is about next gen sequencing.

@Bez I voted to close because I think (a) it is broad (b) I am not able to understand what is OP asking for exactly; some kind of all in one package? I retracted the vote but the question needs some clarification.

There are couple of them. First if you want to sequence analysis basic packages are :
http://www.bioconductor.org/help/workflows/high-throughput-sequencing/
Also, Maqweb seems promising.
http://maqweb.sourceforge.net

Add more software, including commercial, please, if you can


text:
How to do whole genome sequence alignment in R or Ruby/C++, any good language?
I need to perform tuberculosis mutation analysis. First step I need to do is to align sequences in fasta format against one reference file. i tried CLC genomics workstation --- it hangs on 60 000 lines of fasta reference file for entire day. Please advise what technology and tutorial to use to do that task.

I am a poorly trained molecular biologist, so when I build plasmids and have them sequenced I line up the sequences by hand in microsoft notepad. I know it's not a good way to do it, but haven't looked for anything better. What would you suggest for aligning up to a couple dozen relatively short sequences (~500 bases)?

Web VISTA tool designed for short sequences

Found a tool:  MUMmer is a system for rapidly aligning entire genomes.  The current
version (release 3.0) can find all 20 base pair maximal exact matches between
two bacterial genomes of ~5 million base pairs each in 20 seconds, using 90 MB
of memory, on a typical 1.8 GHz Linux desktop computer.
If you know a better programmatic approach, let me know, please


text:
What to do if microarray t-test, ANOVA, SAM and LImma show various selected significant genes?
Need advice: how to approach discrepancy in differential microarray gene expression test results: what to do if ANOVA, ttest, SAM and Limma procedures show different results and especially more discrepant when using log transformations and normalization operations?

I wouldn't expect different methods to give the same results. Further, why are you even testing non-normalized datasets, the results of that are completely and utterly useless for any purpose other than showing that normalization is important. In addition, an T-test is a special case of an ANOVA (and of course limma is itself using a moderated T-test, though it's going to have significantly more power than the others), so I have to ask myself exactly what sort of design you're using that it's appropriate to substitute one for the other and still get apparently vastly different results.
In general, I would strongly encourage you to work with a local bioinformatician or statistician for what is presumably your first microarray analysis, particularly if you don't have a strong statistics background.

We are all academically educated in medicine and computer science, you know. However, we did 7 years of angiogenesis, not microarray research and started this theme recently, We have read many books, and advices are quite controversial. In routine, we do quantile normalization and log2 or log1o transformation for visualization. Design is simple: 4 columns of control bioichips and 6 of experimental data. Problem is that no up- or down- significant expression is achieved when using massive normalization, log transform, FDR and so on. Thank you for helping me.


text:
Retinal eccentricity to colour sensitivity
Colour perception goes out to 50 degrees but is the sensitivity to RGB. Question is it the same in the four quadrants of the retinal field? That is if the red colour sensitivity eg is 30 temporal retina 50 degree nasal retina etc. And what are the eccentric limits for each colour [frequency]in the four quadrants.

Not exactly the same question, but a good reference point in the citations.

I think the PO specifically asks about the differences between quadrants here

Simon: could you clarify your question a bit? As of now it is unclear as to what you exactly wish to know. The linked answer by @anongoodnurse is indeed a very good starting point (and a very nice answer :-)


text:
How much of the human body is processed sunlight?
So I believe (and correct me if I'm wrong--it's logic, not research) that the human body is pretty much all just processed sunlight based on the food chain.  How much, if any, of the human body is made up of materials that did not originate from the sun (e.g., various minerals or other trace elements)?

The atoms in our body do not come from the sun, but the energy to do chemistry on those atoms does. The material itself comes from other stars that exploded over 4.5 billion years ago.

So instead of saying we're made of sunlight, we're really just made of dirt.  Not quite as uplifting.

If you want to be inspired by the dirt remember that it was still made inside a star and then blasted across space by a supernova.

If you want to say it poetically, we're stardust held together by the sun. Condensed and continuously renewed by a giant nuclear forge.

I think that Carl Sagan said it best:

The nitrogen in our DNA, the calcium in our teeth, the iron in our blood, the carbon in our apple pies were made in the interiors of collapsing stars. We are made of starstuff.

The current view of cosmology is that every atom that isn't hydrogen, helium, or lithium was created in the fusion furnace in  the hearts of giant stars. These heavy atoms were then spread about the place by supernovas.
However, there's a lot more to the matter that makes up living creatures than just the atoms. The vast majority of the free energy that allows for the creation of intricate organic molecules with complex patterns of chemical bonds (e.g. protein, DNA, etc.) does indeed originate with our sun.


text:
Aseptic technique: a single technique, or any technique fulfilling criteria, or collection of said techniques?
My friend just used the following sentence in her lab report:

Aseptic technique is used in this step:

I immediately felt something was wrong. She used the term as if it were a specific technique. Is her usage correct, and if so is "aseptic technique" indeed a specific technique with a specific procedure?
Rather, I thought "aseptic technique" referred to any technique that involves complete sterilization of a certain environment or apparatus/instrument. If this were right, then perhaps "an aseptic technique" should be used instead?
Further still, if "aseptic technique" refers to the collection of all techniques that involve sterilization as described above, the perhaps it should have been "the aseptic technique" instead?
Which one(s) is/are correct, grammatically and semantically (hence conveying the concept accurately)?

I bet it means she just used a new pippete

This is more a question about English language and usage than about biology. I vote it be moved to that SE. PS. For what it's worth I think you are wrong, but I'm not going to argue it here.

I'm voting to close this question as off-topic because it belongs on SE English Language & Usage.

Aren't you mistaking antisepsis for asepsis?

@David not sure if I'm conveying it well, but I intended to seek clarification for what the term really means. Is asking for a definition of a biological term that is clearer than what I could find an off-topic question?

@Flo AFAIK you can just sterilize something with fire for aseptic technique, what exactly that means tho is what I'm trying to find out here

I have answered your question. Take note, not only of the answer, but of the way I have supported my conclusions with the results of internet searches for the professional usage of the term. Another time you should undertake research of that type yourself. Although certain scientific terms (mass, current, atom) have precise and unvarying meanings, the meaning of many others — especially when they are in common usage — may vary depending on context. Often the language changes. In English there is no Academy that passes judgement.

This is primarily a linguistic question and I am answering it on the basis that it will be migrated to Stack Exchange, English Language and Usage.
The question is whether, in the context of a report describing (otherwise unspecified) student work, the phrase “aseptic technique” can be used without an article, or whether it requires the definite or indefinite article. This is a question of meaning and usage, and, without using any technical grammatical terms, can be answered by anlysis of scientific publications and by analogy.
“The aseptic technique” (definite article)?
The definite article would normally be used in this type of situation if reference was to one specific clearly defined technique. As an anlogy I would take ‘The Heimlich manoeuvre’ (where ‘manoeuvre’ occupies an analagous position to ‘technique’. Clearly the phrase does not refer to a standard defined procedure like the Heimlich manoeuvre, but merely that the work was performed asceptically (i.e. under sterile conditions). So in this context the definite article is certainly not necesary. In some circumstances employing sterile conditions requires satisfying certain enumerated criteria (example below), in which case the definite article may be used.
“An aseptic technique” (indefinite article)?
I think that this is possible but not obligatory. The use of the indefinite article indicates that the asceptic technique used was one of several possible. Although sometimes this would be used in the context of a limited number of items, this is not a necessary requirement. Analogies with a different adjective would be “she executed the dive with a graceful technique”. Here, the article is (almost) obligatory, but less so in the case of “she showed superb technique in executing the dive”.
“Aseptic technique” (no article)?
As the last example shows (“she showed superb technique in executing the dive”), omitting the article is perfectly acceptable in analagous phrases. I would say it is perfectly acceptable in this case.
The arguments above are only useful to the extent that they reflect actual practice. A quick internet search brought up an interesting example in which both no article and the indefinite article were used in the same text. This is the entry for Asceptic Technique on a website called Healthline.
The second paragraph omits the article:

Aseptic technique is a method designed to prevent contamination from microorganisms.

But when it gets down to specifics:

According to The Joint Commission, there are four chief aspects of the aseptic technique

So unless your friend was referring to ‘The Joint Commission’ (which I doubt) there is nothing wrong with that sentence of her lab report.
Other Professional Examples
ThermoFisher Scientific — no article

Aseptic technique, designed to provide a barrier between the microrganisms in the environment and the sterile cell culture, depends upon a set of procedures to reduce the probability of contamination from these sources

Nuffield Foundation — indefinite article (implied by use of ‘any’)

There are some general rules to follow for any aseptic technique.

ANTT — definite article used in reference to a specific named technique

Aseptic technique is the most commonly performed infection prevention procedure in healthcare; it is also probably the most critical. This article looks at the Aseptic Non Touch Technique (ANTT) model for reducing healthcare-associated infections

(You could argue that the definite article refers to the model, rather than the technique, although I think if you omitted ‘model’ you would be left with an example like the Haemlich manoeuvre. In any case the English in this article is appalling — “infection prevention procedure” gives a foretaste of the stylistic horrors that follow.)


text:
How does heart rate change when entering N1 sleep?
I would like to know how the heart rate changes as a person enters N1 (NREM 1) sleep from a wakeful state. The focus is on entering N1, and it would be great to have time-series data to see the pattern of the decrease, but a  textual description of the decrease would be good too. Most importantly, by how much does heart rate decrease from resting to N1, and how quickly does it fall?


text:
Glycerol 3-phosphate nomenclature
Why is Glycerol 3-phosphate named in such way? Shouldn't it be named as Glycerol 1-phosphate by proper IUPAC- nomenclature?

You're right, according to standard rules of nomenclature it would be called glycerol 1-phosphate. It comes back to the outdated D/L configuration nomenclature. A more thorough explanation is quoted below.

When the R/S system (sequence rule) is applied, substitution of one of the primary hydroxyl groups often leads to changes in the configurational prefix, thus obscuring chemical and biogenetical relationships; it is generally inapplicable to the steric description of such mixtures as occur in triacy1glycerols isolated from natural sources. The stereospecific numbering of glycerol and its derivatives as proposed by Hirschmann [9], described above and in 1, avoids these difficulties; it has proved useful and is widely accepted.

Source.


text:
What is the field of view for the human eyes?
I'd like to know how much a person can see regarding the angles.
If it is a rectangle, I'd like to know it's height and width.
But if is another shape, I'd like to know which kind of shape and the angles.
I suppose that we can see something like this and if this is true I am curious about 4 dimensions:

"vertical" angle for both eyes
"horizontal" angle for both eyes
"vertical" angle for an eye
"horizontal" angle for an eye

It would be also nice if there will be some "areas" with percentages. I mean, something related to "central" vs "peripheral" view, because we see better something that is in front of us than something that is near us.

The general shape of the field of view has been answered in the related question "If human eyes watch an area, what's the shape of its capturing shape? Rectangular? Half spherical?"
Regarding the central view: yes, foveal view has a higher acuity than peripheral view.
Regarding the numerical dimensions of the monocular and binocular field of view: Monocular field of view  (measured from central fixation) is 160 deg (width w) x 175 deg (height h). The total binocular field of view is 200 deg (w) x 135 deg (h).
The region of binocular overlap is 120 deg (w) x 135 deg (h) (WebVision). The binocular foveal high-acuity part (central view) is about 6 degrees (5-15 degrees).

Chris what does the w signify in the brackets? Does it stand for width and h for height? Or does h stand for horizontal and w meant for vertical?

w x h = width x height, question edited. thankx

Good answer so +1. Though it would be more useful if you can split the monocular vision angle in horizontal direction as nasal and temporal fields

@CRags - the linked question covers nasal/temporal aspects. And thanx :)

Sorry, I didn't check that question Chris

One thing that's interesting is that the optical system is not just encoding image feature details (like a camera), but also has built-in low-level filtering that can detect motion with reduced latency compared to the pathway used for feature detection.  This is relevant when considering vision as an ongoing process, since the eyes are typically constantly moving, with a choice of focal point partially motivated by motion detected in the periphery.


text:
Can memory be improved with mental training?
I am a man in his mid thirties, but I already have a pretty bad memory. (I have always had a bad memory.) I can remember certain kinds of facts and music very well, but when it comes to words or even random  stuff like how did I fix a particular issue when I last encountered it, my mind goes blank. Lack of sleep aggravates it even more. Lack of sleep also severely retards my language skills because I can't recall any vocabulary. Other than the memory issues I am a healthy person. Is there anything I can do to improve my memory?

Welcome to Biology.SE! This post would be a better fit on CognitiveSciences.SE.

I'm voting to close this question as off-topic

You are not alone.
I think most people do not use the memory capacity of the brain optimally.
Some people use it more optimally than others though.
The researchers who wrote the book "Make it Stick" researched exactly this problem.
Of their many excellent findings, I think the most important was that most people did not convert the knowledge that they accumulated in working memory into long term memory because they did not do spaced repetition of recall practice.
When we learn something new those synaptic connections are weak unless we strengthen them.
The brain seems to let go of information that it deems to be less important in this fashion.
Everybody forgets a little.
But if you practice recalling what you've learned at spaced intervals, that seems to greatly improve the ability to convert working memory to long term memory.
Its important that recall involve actually struggling to recall the information.
Its the struggling that seems to strengthen the synaptic connections.
Just rereading some material wont work.
I put everything that I learn into Q&A documents that I use for recall practice.
This seems to have significantly improved my ability to commit new knowledge to long term memory.


text:
How to study the number of herbivores per type of tree and time of day?
Suppose I want to find out the number of herbivores in different kinds of trees, and also compare the numbers between day and night. How would this kind of study be run in practice? It easy to think of several possible confounding factors, such as the health of the trees, weather, etc.
If the trees are big, it is also difficult to find every living thing from that. One could of course then count the number of herbivores per defined area but again, picking the area should be carefully controlled.
From a statistical perspective, I can just make an estimate of expected effect size, and calculate the sample size that is about enough for detecting possible differences in the above mentioned conditions. However, I find these other aspects very difficult to do... All help would be appreciated :)

I think there are a lot more factors you need to provide before someone will give you a helpful answer. What trees are these, what herbivores are you studying for example?


text:
Do these things contain amylase?
I have 10 samples of some food or other things and I need to know, if it contains amylase. I already ran an experiment with storch and iodine, but I have to make it right and my experiment must not be right.
List of samples:

Saliva (I know this one)
Banana peel (inner side)
Corn
Sponge biscuit
(http://www.kaloricketabulky.cz/fotografie-velka/f1136aba2e11082a/piskoty-detske-kulate.jpg)
Tomato
Banana (dried)
Bread
Potato peel
Ketchup
Milk

Thank you very much!

What was the problem with your experiments? You can't trust your results, why?

Because I dont know if I did it right. And for example potato peel colored something between iodine without starch and iodine with starch.

This sounds like a piece of homework. An important thing to learn in science is that you have to take the results for what they are - though the experiments should be arranged so that they could convince you i.e. repeating 3 times or something similar. Negative and positive controls are used to test whether you did it right. http://en.wikipedia.org/wiki/Scientific_control#Negative

you can also compare your results with that of your fellow students to improve reliablity and eliminate subjective bias

Amylase is an enzyme that breaks down starches to simpler sugars. Only living organisms can produce amylase. Animals produce only alpha-amylase. Plants, bacteria, and fungi produce both beta- and alpha- amylases. Like all proteins, the presence of amylase in food depends on if it is permanently denatured by high enough temperatures or extremes in pH. Interestingly, amylases can be classified into high/intermediate/low thermostability groups, depending on whether they become inactivated at a certain temperature. Taking this into consideration, saliva would definitely have alpha-amylase. Bread and biscuits may have alpha or beta amylase (depending on baking temperatures/pH, if amylase was added at all, and if it comes from a grain). Of the rest of your list, banana, corn, milk, and sweet potato would have amylase. Honey (not listed) would also have it. Tomato seems to amylase activity as well. For ketchup, it seems to be an added ingredient to speed processing.
Sources:

http://www.gmo-compass.org/eng/database/enzymes/80.amylase.html
http://www.lallemand.com/BakerYeastNA/eng/PDFs/LBU%20PDF%20FILES/2_7SOFT.PDF
http://www.ehow.com/info_12013063_plants-contain-amylase.html
http://www.ajofai.info/Abstract/Detection%20of%20amylase%20activity%20from%20vegetables%20and%20fruit%20in%20an%20undergraduate%20classroom.pdf

but yeast zymase is not amylase?

@CRags, yes you are right! yeast can make amylase too though, I believe, but zymase is the more active enzyme in yeast. bad example then on my part.

I didn't know yeast can make amylase. Thanks for the info. Thinking on banana, it makes sense if amylase is present in it (as it's sweet, it must have a lot of glucose).


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How many photosystems in a chloroplast?
I haven't been able to find any good order-of-magnitude estimates for how many photosystems (e.g. how many PSII complexes, how many PSI complexes) are in an average chloroplast (or perhaps per area of thylakoid membrane).
Textbooks always just show a small area of membrane, and I'm interested to know whether there are say hundreds of complexes or millions. Is there any published data on this?

This article states that in plants at 15-25% relative water content (RWC), the PSII density is around ~700 complexes/µm$^2$, and in hydrated plants ~1500 complexes/µm$^2$.

They also have some nice Cryo-SEM images of grana membranes and the changes in PSII complexes density depending on their RWC. Which is also an important aspect of the question, since the amount of PSI and PSII complexes will vary depending on the environmental stimuli.

Additionally, given that biological material is variable even within the same species (different tolerances might have a different effect on the amount of complexes/µm$^2$), I would expect variability in the complexes density among different species of plants too.
Regarding PSI, I found an article where mass spectrometry analysis approximates the average of PSI in the thylakoid of a Prochlorococcus MED4 ecotype to 4303/μm$^2$. However, the thylakoids of another ecotype had more densely PSI organizations of crystalline pseudo-hexagonal arrays and the average was estimated at 5583/μm$^2$. In fact, the article tested growth under different conditions (low-light, high-light, poor-nutrient) of the different ecotypes and supports the hypothesis that the second ecotype adapted to low-light conditions (by maximizing the amount of pigments in its thylakoid membrane) while the first one adapted to high-light conditions. In this case, the observed part of the membrane with cryo-EM tomography was ~6 μm$^2$and ~22 μm$^2$ of thylakoid membrane area for the first and the second ecotype.
I think the right answer is that there are many factors affecting the distribution of PSI and PSII that are still unknown and a better approximation cannot be made.

References
Charuvi, Dana & Nevo, Reinat & Shimoni, Eyal & Naveh, Leah & Zia, Ahmad & Adam, Zach & Farrant, Jill & Kirchhoff, Helmut & Reich, Ziv. (2015). Photoprotection Conferred by Changes in Photosynthetic Protein Levels and Organization during Dehydration of a Homoiochlorophyllous Resurrection Plant. Plant physiology. 167. 10.1104/pp.114.255794.
MacGregor-Chatwin C, Jackson PJ, Sener M, Chidgey JW, Hitchcock A, Qian P, Mayneord GE, Johnson MP, Luthey-Schulten Z, Dickman MJ, Scanlan DJ, Hunter CN. Membrane organization of photosystem I complexes in the most abundant phototroph on Earth. Nat Plants. 2019 Aug;5(8):879-889. doi: 10.1038/s41477-019-0475-z. Epub 2019 Jul 22. PMID: 31332310; PMCID: PMC6699766.


text:
How frequently does recombination occur, and how long are the recombinated fragments?
I understand the mechanics of recombination, but am struggling with the 'scale'.

When two homologous chromosomes pair, roughly how many recombination events occur on average? I understand there will be a distribution, and it will vary between species - but are we talking one, two, or hundreds/thousands?

How are long are recombination fragments relative to the entire length of the chromosome? With the same caveat as above, I'm trying to get a sense of scale - 0.001%, 1%, 10%, 25%?

When crossover happens, it's a whole swap from that point on, not just a little chunk. So if there's only one crossover event, then the lengths are "p" and "100% - p", where p is the position along the chromosome. The only way to get a small piece of one chromosome amidst a mostly intact copy of the other would be for there to be two crossovers close to each other.
This existing Q&A talks about the rate of crossovers in human chromosomes:
How many recombination events are there per generation in humans?
It varies by which chromosome you're talking about and other factors, but something along the order of 1 to 4 events per chromosome would be a reasonable ballpark. 0 is possible, too.


text:
Do both a separate B and T lymphocyte need to be activated during the immune response?
Isn't it very unlikely that there will be both:
a) a B and a T with a receptor complementary to the antigen, and
b) that they will come into contact with the right antigen-presenting cell?
What would an immune response look like with only a B lymphocyte or a T lymphocyte activated? Is there any way for one class of lymphocytes to 'transfer' the complementary receptor to the other class?


text:
Evolution experiment for kids?
What would be a good plant to show the process of evolution to a small kid? Obviously it's a long term experiment, and preferably a fruit or a veg that is edible (like tomato?), and what characteristic would be (size, colour) good to select for?

How old is "kids" in this question?  I could imagine a thorough answer would address different suggestions for ages 4-5, 9-11, and 16-18, say.

You are going to need an organism that has a very short generation time to make an evolution experiment. Fruit flies, yeasts, E.coli. are classic examples. It is going to take a few years to have only a moderate response if you use tomatoes. Also I doubt you can really control tomatoes reproduction.

What exactly are you trying to demonstrate? Just the response of the mean phenotype to a threshold selection you would make?

Kid is 4, run the experiment for a decade. I thought (likely wrongly - this is just a layperson's wish to encourage science in the kid!) initially in the 19th the experiment was done with some kind of pea? I wish to demonstrate selection pressure - choose for a characteristic, see the result in the future. (If I'm being dumb tell me, I'll delete the question! :) )

@IlyaGrushevskiy 10 years is probably a bit long for the attention span of a 4 year old. :) I think if you change your question to demonstrate natural selection then there are some easy experiments that can be done on the order of an hour or so and are a bit more hands-on than waiting for plants to grow.

I'd say you will be better off writing a computer simulation (e.g. a very basic  genetic algorithm) with the child. This will demonstrate the same process and will expose the child to programming and some light maths. Both things are good to be exposed to at an early age. A 4-year old child is perfectly capable of understanding the maths behind basic random processes and computer code.

(you can check out the game I suggested here: https://biology.stackexchange.com/questions/54106/pen-and-paper-game-to-explain-the-theory-of-evolution/54107 - that question was closed at the time for being too broad, though. Similar to yours, it's a bit broad to focus on 'evolution' in its entirety)

If this option suits you, I can write a short example as an answer.

This Scientific American article may be of interest: https://blogs.scientificamerican.com/psi-vid/an-evolution-animation-unlike-any-youve-seen-before/.

This is for an animal, not a plant. But, when I was in school, the Peppered moth was used as an example of rapid evolution from the 19th century. Its white coat made it very noticeable against soot-stained surfaces so it had a rapid selection pressure to become black. If you can organise a trip with your kid to a natural history museum, you might be able to find some specimens.


text:
Why do we do nested PCR?
Wikipedia:

Nested polymerase chain reaction (Nested PCR) is a modification of
  polymerase chain reaction intended to reduce non-specific binding in
  products due to the amplification of unexpected primer binding sites.

I understand that there are two steps and one of those steps involves a non-specific primer followed by a specific primer...
But this does not seem to have sense. What is the purpose of running a non-specific PCR just to hit it with a specific primer afterwards?
What do we gain when doing a nested PCR?
Practical example:
We are planning on sequencing human skin microbiome. Would the ratios of different bacterial species differ if we would use the nested PCR products for sequencing, as compared to standard PCR?

If your initial template results in multiple amplicons that cannot be removed by increasing annealing temperature, nested pcr can reduce these amplicons when coupled with a gel extraction.

To extend on @MarchHo comment, nested PCR is used for the amplification of a target when too many non-specific fragments are produced by direct PCR. Usually you would use a nested PCR when 1) the sample is complex (multiple DNA sequences) and your target is present in a very small amount as the target would not be amplified otherwise, or more precisely a direct PCR would produce way too many non-specific fragments. 2) When you have many non-specific fragments as a first PCR amplification enriches your "real target" sequence.

Thanks cagliari. If you could write it as an answer then I would gladly accept it, because it answers my question

In the paper by K. Lily Therese, U. Jayanthi & H.N. Madhavan traditional PCR wasn't sensitive enough to allow for an accurate reading on what they were trying to study. By using nPCR they were able to amplify around the gene they were interested in and then amplify just the gene they were interested in for a more accurate and sensitive study. The successive PCR allowed them to amplify their specific gene even if there was only one copy in the sample.
I recall using this procedure in Molecular Genetics Lab, it was used to make sure that our sample was purer.

It may depend on which protocol you looking at, but you can use a specific primer set for the first PCR and another specific primer set for the second PCR.
Even if you use a none specific primer set for the first PCR, it could be easier to amplify your target sequence because your target sequence would be more abundant than the original solution before the first PCR is performed.


text:
How to calculate biological half life of a drug that is dose dependent?
I would like to calculate the half-life of a biological drug.
This biological drug is said to have a biological half-life of:
3.33 days when a patient is receiving a dose of 0.04 mg/kg of body weight,
13.4 days when the dose is 0.2 mg/kg
and 14.9 when the dose is 1 mg/kg

How could I extrapolate this information to get biological half-life estimate for 2 mg/kg of body weight?
Could I also graph this? for example in R?

This sounds a lot like a homework question. I'm glad you got an answer though.

Maybe it does but I'm actually a doctor and I have a patient that has to switch from one clinical trial to another. He may go into the second clinical trial only after a wash-out period of 5 drug half-lifes. and the information I have given - is actually in the drug description.

I plotted your data using MATLAB and it looks like this:

Most degradation or clearance processes happen via first order kinetics. However when the clearance/degradation machinery gets saturated then degradation proceeds via a zeroth order kinetics i.e. it becomes independent of the concentration of the drug. The half life in first order reactions is independent of the initial state. Only in the case of the zeroth order reactions, the half life is directly proportional to initial state (See here). In this graph there is a huge gap in half life, between the first and the second points. We need more data points to say anything conclusively about this observation. However, I am assuming that the clearance reaction is already in the zeroth order kinetics as half life increases with concentration (though at different rates). For a rough calculation let us consider second point onwards. By calculating the slope between second and third points you can obtain the half life corresponding to dosage of 2mg/kg.
$$Slope=\frac{t_3 -t_2}{x_3-x_2}\\ t_4=x_2+slope\times2=17.15\ days$$
There can be other complicated explanations too, such as the drug inhibiting its own clearance etc. But for assuming such models we would require more information.

does it mean that more drug "clogs" kidney (for example) so that drug stays in blood stream longer? Is it real effect (observable in reality)?

@aandreev I haven't studied that with drugs but if you overexpress proteins beyond a limit then their degradation rates become zero order i.e. independent of concentration of the protein because proteosomes get "clogged". Same goes with drugs and if two drugs require same enzyme for their metabolism then taking them together may be harmful. I guess, that is why most drugs are metabolized slowly when someone has consumed alcohol.


text:
Where to find gene manipulation video (or photos)
I hope Im not asking a dumb question!
Where can i find video of gene manipulation in action under microscope?
Like extracting a gene from a cell, fixing gene mutations, putting the gene in a vector, that kinda stuff. Is this too small to show in video or photos?
If i look up youtube all I find is scientists using lab machines and equipments except for under miscroscope!!!

There are no videos of that, since you cannot see the DNA you are working with unless you precipitate it in large amounts.

You can find videos of microinjections, but you're not actually going to see DNA.

Like this video http://www.dnatube.com/video/5561/What-is-Blastocyst-Microinjection

Ok now I understand thanks! So how do scientists manipulate genes if they can't see what they are doing!??

The comments effectively answer the question. There is no need to close it as broad. The main question here is "Is this too small to show in video or photos?" which can be answered. I am voting to leave this open.

From the comment section:
We don't have to see the actual changes. It's like chemists who will mix compounds together and obtain a new molecule. They dont see the chemical reaction per se but can test the new molecule to make sure what they predicted would happen had happened. Finally we often use fluorescent proteins to track some of the modification performed (which could involve a microscope). For the how, well that's a bit broad and involves too many notions to make a summary here.


text:
Transformation efficiency
I accidentally spun down the cells after heat shock treatment before adding the media into the tubes while doing transformation? will the transformation work?

The protocols for preparing competent bacterial cells all involve concentrating log phase cells and incubating them on ice in the presence of divalent cations.  There are many different recipes for the buffers, time of incubations, temperatures, etc. What could an extra centrifugation step do that would harm the experiment?

The question is following: did you incubate cells on ice before spinning? Protocol, for example this one for $DH5\alpha$, calls for just 10 minute incubation after heat shock:

Heat shock at exactly 42°C for exactly 30 seconds. Do not mix.
  Place on ice for 5 minutes. Do not mix.
  Pipette 950 µl of room temperature SOC into the mixture.

Did you centrifuge your tubes after step in bold?
My bet is that spinning cells down (taking into account what @chris wrote about centrifugation parameters) will not dramatically decrease efficiency of transformation. DNA should be already in cells after step, highlighted in the quote.

This is hard to answer since we don't know the exact conditions you chose, as these are rotation speed (or better g), how long you spun them down and also if you used a cooled centrifuge or not. It's also important how gentle you resuspended the pellet.
However, I would plate these cells, no matter what happened since you are at the last step of the procedure and have nothing to loose. Do the usual dilutions you use for plating your cells and then add another plate with undiluted transformation mix. If you have only very few surviving cells after your mistake you might get your clones on this plate. If it doesn't work, you will have to repeat the transformation.


text:
What's the proton concentration around a DNA helix?
Let's suppose the concentration of a 20-nt DNA strand is $10^{-4}$M and the solution does not contain any salt ions. In a solution with pH 7, $[H^+]=10^{-7}$M, on average each DNA has only 0.001 protons. But the DNA phosphate groups become charged through de-protonation so each DNA should effectively release 20 protons thus we would expect $[H^+]=20\times 10^{-4}$M. How does the system maintain chemical equilibrium while keeping charge neutrality? If $[H^+]=10^{-7}$M because pH=7, where do other protons go?

If you added DNA with a protonated phosphate backbone to a sample of pure water with pH of exactly 7.0, the extra protons on the backbone would be picked up by waters to create a deprotonated backbone and hydronium ion. The charge is still balanced, the backbone becomes negative and the hydronium is positive. The pH would change, becoming more acidic, I don't know how acidic, depends on the amount of DNA and equilibrium constants, and I don't want to do that math right now.

I'd suggest specifying in your question that your system is just water at some sort of default conditions.

 DNA stands for deoxyribonucleic acid. Acid, by definition and mechanism in aqueous environment, is something that donates proton ($H^+$). HCl dissolved in water will donate proton to solution, thus bringing pH down, since $pH=-log_{10}[H^+]$.
DNA, being an acid, donates protons to water and brings pH down a notch. Just like in case with HCl, it has nothing to do with keeping charge neutrality. Water is not a buffer, that is able to tolerate or smooth change in pH. What happens when you add DNA to buffered solution, say phosphate buffer, is completely different story from biochemistry.

Note that DNA also has "bases".. But since they are paired, they may not contribute to basicity.

indeed. Single-stranded DNA will act differently

The nitrogenous bases are Lewis bases (that can donate an electron pair) and are extremely weak, similar to pyridine.

Since DNA is an acid it is reasonable to ask: what is the pKa of the phosphate residues located all along the polynucleotide's sugar-phosphate backbone? Apparently that number is at a pH between 1 and 2 (http://www.bio.brandeis.edu/classes/biochem104/DNA_lecture.pdf). That  means at physiological pH ranges (for example, the pH found inside the nucleus or cytoplasm of a cell, around 7 or so) 100 % of these phosphates would be ionized (unprotonated), and therefore strongly negatively charged.  The counter ions would be any suitable mono- or divalent cations handy. When you purchase intact DNA the fibres are typically the sodium salt--I believe this is similar to the material Wilkins & Franklin used to obtain the images Watson & Crick used to solve the structure.
So strictly speaking, the experimental situation described in the question does not exist. You could never obtain a pure sample of protonated DNA that you could then add to pure water. At the pH the DNA would be protonated the DNA would depurinate leading to strand scission at the abasic sites.  This is the whole principle of soaking your agarose gel in HCl in preparation for a Southern Blot, to fragment the high molecular weight fragments so they will migrate more efficiently out of the gel and onto the blotting membrane.

nice expansion of original problem!


text:
Ions in different cell compartments
I would like to understand the distribution of metal ion concentrations (such as Mg2+) in the different cell compartments. I tried very hard but still couldn't find such information. Could anyone help?  Also, could you recommend a good reference on this problem? Thank you!


text:
Is the structure of human brain white matter fixed at/near birth?
I have been reading that, with exceptions for a few parts of the human brain, no neurogenesis occurs, so no new neurons are created.  I have also heard that no new axons are formed through the white matter of the brain after birth as well.  I also know that the axons are myelinated, minimizing crosstalk and other interesting structural effects that might occur.
Between those, does that imply that the structure of the white-matter of the brain is fixed at a very young age, and never changes through our life?  It seems like a natural conclusion from the data, but it feels counterintuitive when contrasted with the continuous creation and destruction of synapses which happens so close nearby.

No, white matter structure is not fixed at a very early age. Although a person is born with most of the neurons they will ever have, those neurons must form connections between each other, via axons and synapses, and many of the axons become myelinated during this period. Although the number of neurons remains relatively constant, these processes lead to a substantial increase in overall brain volume. After a few years, there is then a period of synaptic pruning (https://en.wikipedia.org/wiki/Synaptic_pruning), in which many of those connections are rationalised. These processes explain many of the characteristics of human development.
For example, mammalian species can be characterised as precocial or altricial. A precocial species is one in which much of the brain's development has been completed in utero. This allows for a relatively sophisticated behavioural repertoire to be immediately available (think precocial = 'precocious'). For example, a foal is born and almost immediately is able to walk, follow its mother, and so on. Meanwhile, an altricial species like a human is born in a relatively helpless state, incapable of independent locomotion and with even very limited perceptual processes. It is the development of axonal and white matter pathways, with associated synapses, that allow learning and development of new skills in the post-natal period.
During this process, the brain is extremely flexible. For example, a baby can initially distinguish between the phonemes of any language. As its white matter connections develop in response to a lot of exposure to the language(s) in its home environment, the brain becomes more specialised. Eventually, past the pre-teen period, it becomes much harder to perceive and articulate subtle phoneme distinctions from other languages, and the acquisition of new grammars shifts from effortless and rapid, to slow and requiring formalised instruction rather than being spontaneous.
This shift to relative inflexibility reflects the second phase of white matter development (i.e. large-scale synaptic pruning). That is, in the first phase, there is widespread growth of connections between neurons via axons and synapses, along with myelination. In the second phase, the flexibility of this system is traded for the efficiency and focus of a brain that has learned what specific abilities it needs to have. This continues up until about age 10, at which stage 50% of the synapses present at age 2 have been lost (https://link.springer.com/referenceworkentry/10.1007%2F978-0-387-79061-9_2856). Learning is then no longer so rapid, but with specialisation and development, an adult is able to focus attention explicitly and maintain discipline towards achieving goals, where a child might get more easily distracted and seek novelty.
Synaptic formation and loss then continues throughout life, as the underpinning of learning processes, but no longer on the mass structural scale seen in earlier development.

Is it only the synapses that are changing, or are the long axions also growing or changing, such that they might terminate somewhere else in the brain?

It is probably the competitive selection and destruction of axons that is the dominant process. eg in the adult macaque there are 50 million axons in the corpus callosum, selected from the 200 million available at birth. Check out chapter 6 of this textbook by Ackerman for a good introduction: https://www.ncbi.nlm.nih.gov/books/NBK234146/?report=reader#ddd00050


text:
Are the destruction of Olfactory Receptor Neurons (ORNs) permanent?
I lost the ability to smell a particular smell due to an exposure to solvents years ago.  It has never fully come back.  I had always assumed that simply meant I had permanently destroyed my ORNs for that smell.  However, I have recently read that ORNs are replaced every 60 days.
Is it possible to lose all ORNs for a smell and have them never come back?  I'd love to know whether my long term loss of smell is due to something cognative, or whether it is a complete lack of inputs from the nose.

I'm confused by what you mean when you say "something cognitive". Do you mean central nervous function?

@anongoodnurse I am referring to something dealing with the processing of the information, rather than the part which generates the information from the stimulus in the first place.

I would suggest that you remove all personal references and simply focus on the question on "whether ORs regenerate"

@WYSIWYG Is that a preferred way to do things on this stack exchange?  On some of the SE's I frequent, the personal reference content can be useful for trying to work through any mistaken terminology that might come up in the objective part of the question.

@CortAmmon Yes; when you explain the context of a terminology that you might have encountered but personal experiences such as this one do not provide any context. It is not necessary for others to know about the incident in order to answer your question on olfactory receptors. Whatever your sensory perceptions are, after the said incident could be simply idiosyncratic and are therefore considered as an anecdotal evidence. Your personal reference just makes the reader think that you are just asking about what happened with you, which I believe is not really the case. Hence the suggestion.

You can add a line on your personal observations IMO it is better if you do it after explaining the question properly. For e.g. I read that ON regenerate [cite reference]. Are they always regenerated such that an odorant perception is never lost... ... I have not come across any study but based on my personal experience ... and so on.


text:
Why does rapid decompression make you lose useful conciousness so fast?
I was watching Smarter Every Day's episode on hypoxia, and it had an interesting chart that suggested that at 35kft, you have less than 10 seconds of useful consciousness.  This number seemed low, and I'd like to know why.
I have two pieces of evidence that make me question the chart (even though I know Destin from Smarter Every Day doesn't make mistakes lightly):

I can hold my breath after an exhale and function for well more than 10 seconds
It seems to me that the vacuum of space would be the ultimate test for how long you can sustain consciousness without oxygen, as the vacuum of space literally strips oxygenated blood as it passes through the lungs.  Wikipedia cites sources claiming you go unconscious in under 14 seconds, and a case of accidental vacuum exposure that resulted in a loss of consciousness in 15 seconds.

So why is it that the "useful consciousness" table seems to contradict these datapoints?


text:
Are there biological ratchet cycles that are small in number?
I recently came across the strange factoid that all animals that can jump do so to roughly the same height (within an order of magnitude).  The argument was that the work done by muscles in a single contraction is proportional to their mass, and the amount of energy required to jump is also proportional to their mass.  The secondary issue of power could be solved by an approach like the click-beetle uses, where they store the energy in their shell slowly, then release it quickly.
I'm an engineer, so my first thought is that a ratchet could be used to circumvent this sort of limit.  If I could cycle a muscle 2-3 times and use a ratchet to store that energy, I could release 3x more energy and jump higher.  As an engineer, it seems like a no-brainer.
But I can't seem to find any biological example of such a ratchet.  The closest I could find was the muscle proteins that cause contraction in the first place.  But that didn't fit the image of the structure I cared about because it was literally millions of these ratchets and the result felt "too smooth" for the concept I was searching for.
So my question is whether biology has a structure that operates like:

Powered by a muscle that gets to contract multiple times (or another chemical process which cycles a small number of times. 2-10 is fine, 10 million is not)
Stores the energy of each contraction
Releases that energy in one burst.

Mentally I'm thinking of a ratchet that I could crank down with 3-4 pulls of a lever, and then release all that energy at once, but I'm open to other biological structures which meet the above requirements.

It's a very interesting concept, the only thing I can think of that's at all similar is neurons, which slowly gain charge, then release it when they transmit the signal.

Do contractions for giving birth count? :)

@Armatus It's not quite what I had in mind, but it sure is darn hard to argue that it doesn't count =D  As I commented on your answer, I was looking at jumping heights and the rapid explosion of energy needed to jump higher, but contractions certainly are using a ratcheting like motion... just to gain mechanical advantage rather than storing power!

First I would in return ask why the actin-myosin coupling should not qualify - the many repetitions of this contractile unit never contract at exactly the same time, and their combined contractile force certainly accumulates in a ratchet-like fashion across the microsecond time scale (with other units contracting before previous units have relaxed). Just because it's a lot of them doesn't make it less ratchet-like :)
With this restriction though, and looking for a "macro-scale" example, I am not aware of anything fitting your description. If I think about it as follows, it also seems intuitive that this wouldn't evolve.
A ratchet as you describe, let's say able to store up x contractions of a muscle for instantaneous release, can also be thought of as a series of x muscle contractions coupled in series across time. It would be equivalent in output to coupling x muscle contractions across space and executing all of them simultaneously. In other words, growing x times the muscles achieves the same benefit.
When it comes to the probability of evolving, what's more likely: an entirely new mechanism to store mechanical energy across time and allow building up, or a simple duplication of the same tissue? The currently existing muscles answer this question: duplication. This can be seen in the different structures that muscles have across living species (muscles in animals, similar contractile mechanisms elsewhere).
The smallest contractile unit in muscles are myosin heads coupled to actin filaments. Duplicate this unit (repeatedly) in two dimensions of space to obtain a myofibril. Multiply the myofibril many times and you reach a single muscle fibre. In fruit fly larvae, this is where it stops - each muscle consists of a single fibre. By the time you're at the adult fly though, the muscles that power the wings consist of a handful of packed parallel fibres. As you go down other routes along the evolutionary tree towards the mammals, you end up at muscles that consist of masses of fibres packed into fascicles, of which many are packed into an individiual muscle. As described above, at each level you have a "many-ratchet", because fibres and fascicles don't contract at exactly the same time everywhere.
So yes, you could evolve a ratchet. Or you could just evolve a bigger muscle. If many animals happen to stop evolving more muscle at around the same absolute potential jump height, that to me suggests that this is a universally beneficial jump height to evolve for terrestrial animals regardless of body size.

Even the fastest striking animals we know of (mantis shrimps) don't use a ratchet mechanism. They do have to 'lock' their muscles though (with some sort of spring mechanism) in oder to release all the energy build up by muscles in a minimised time window. https://www.nature.com/articles/428819a

The reason I don't count actin-myosin is because my particular interest is in jump heights.  The maximum jump height for an animal turns out to be constant, whether you are a mouse or a cheetah.  It's limited by how much energy a muscle contraction can bring to bear divided by the mass of the muscle.  I'm looking at how to store mechanical energy in other forms that could escape this limit.

Even with a constant maximum power output per gram of muscle (which is basically the limit imposed by the nature of actin and myosin as a contratile mechanism), there should still be the ratio of jumping muscle to remaining body mass as a limiting factor that could be tweaked to evolve higher jumps.


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50-400 bps consciousness: why do we draw the line there?
I have found studies that suggest the human consciousness can process 50 to 400 bps.  The exact number varies, but it's always quite small.  It is usually associated with some test results, but how do they decide where to draw the line?  How do they argue their test is the right one?  Is there some strong knee in the curve, or maybe a brainwave being detected which we recognize as occuring with conscious thoughts but not unconscious thought?

You'll have to read the individual papers. Personally I find these not to be very useful or meaningful measures. Brains aren't computers, they don't process bits.

Stating generalizations about consciousness is crazy because, while the conscious mind can process a small amount, the brain has like an L2 cache, a secondary level of consciousness that is immediately available if necessary... Consider you senses can record 2-3 megabytes per second of sound, image, and other information. secondary subconcious processes make that data available to the conscious process if necessary, and it's more about what we choose to ignore than what we have the power to focus on. we have a vast amount to data which is nearly in focus and available for deliberate thought.

The brain also has culture, so the 400kb of concious thought is built on a previous library of 10gb of best reactions for a given time, it's like a processor that builds itself, so a guy playing tennis or driving a car, processes huge amounts of previously concious thought automatically.

For the benefit of many if not most readers could you add at least a bit of background of what bps is and how it applies to human consciousness, if not some evidence of prior research beyond the unsupported "I have found studies..." Thanks!


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How much energy can one muscle contraction deliver?
How much energy is available in a single muscle contraction?  I'm guessing the correct units are J/kg, but I'm open to more correct units.  I'm looking for work done, not total energy dissipated (not interested in heat)
The goal of such a number is to figure out an upper bound on how much work a human body can do if it is never permitted to reset a muscle by moving the limb in the opposite direction (If the bicep does work for this test, the triceps isn't permitted to contract to return the curled arm back to its initial straight position)

This question needs substantially editing to make it at all answerable ~ different muscles in a body are different sizes ~ the same muscle in different people are different sizes ~ the size of a muscle necessarily impacts on how much energy it can exert ~ so "one muscle" means almost anything in that sense.

@Pelinore That's why I said I believe the correct units will be J/kg, which resolves that issue.  However, I'm open to other units which are more correct for making such measurements.

Ah, fair enough.


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How fast can muscle fibers relax
I can find a great deal of information about how muscles contract, and how we divide them up into fast twitch and slow twitch and so forth.  However, I can't seem to find anything on how fast a muscle fiber can relax.
How fast can a contracted muscle fiber stop providing force when the motor neuron stops innervating it?

To clarify, are you sure you mean to ask what happens when a "motor neuron stops innervating" a muscle? Or do you mean to ask about the normal physiologic process of muscle relaxation.

I thought they were phrasings for the same thing, but perhaps I used the wrong term.  A physical example of what I mean:  I am doing a bicep curl.  At a point near the top of the curl, I relax my muscle as much as possible and let the weight (and my arm) fall.  I'm interested in how quickly my muscle can stop resisting that falling movement.


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Are there known counterexamples to Hennman's size principle for muscle unit recruitment?
It is known that generally muscle units are recruited from small to large, and that typically also means slow to fast twitch.  This principle is called Hennman's size principle.
I've seen many articles backing this claim up.  However, I'm curious if there are any known situations where this principle is known to fail.  (Perhaps when there is a known impulse arriving shortly and it needs to be opposed by large fast-twitch muscle).
All I have found so far are articles which agree with the principle, but it seems surprisingly simple for a biological system.


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Do neurons that *don't* fire together unwire?
We all know the classic Hebbian theory, often phrased as "neurons that fire together wire together."  I'm curious about how other connections get pruned when two neurons start to fire together.
If two neurons start to make a strong connection and fire together often, will they prune connections to other neurons faster than if they were merely "dormant," becoming more and more selective towards that channel.  Or is the result simply a more connected structure and the pruning of connections continues to occur at the usual pace?

"Specific" unwiring via timing
A more modern understanding of the classic Hebbian aphorism is spike-timing-dependent plasticity. It is observed that connections are strengthened or weakened according to the relative timing of spiking and inputs. Specifically, synapses that are active shortly before a cell fires an action potential tend to be potentiated ("wire"); synapses that are active shortly after a cell fires an action potential tend to be depressed.
So it isn't just that cells that fire together wire together, it's that cells that fire together in a certain way wire together, and cells that fire together in another way "unwire". I think it's important to recognize that a reduction in synaptic strength doesn't necessarily mean immediate loss of a synapse. Weak synapses are common, and only the very weakest are pruned entirely.
Non-specific unwiring via homeostasis
Another general principle, which may be closer to what you are thinking about, is homeostatic plasticity including synaptic scaling. Just like other physiological processes are under homeostatic control, neurons tend to adjust their responses to maintain an overall activity (firing rate) homeostasis. This process occurs on many different time scales and systems, but stated generally, high levels of activity in neurons tend to activate cellular processes that will reduce future activity, and low levels of activity tend to activate processes that will increase future activity.
Current thinking is that synaptic scaling occurs generally rather than specifically. By increasing the strength of specific synapses via Hebbian plasticity and at the same time slightly decreasing the strength of all synapses, the overall balance of input stays about the same (homeostasis).
Of course, things are a bit more complicated when you look over the whole nervous system and the whole time course of development through adulthood, but I think that's outside the scope of this answer.


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All-or-nothing-law: law or general principle?
The all-or-nothing principle indicates that a nerve cell fires at maximum potential or not at all, based on a threshold on the stimulus.
Is this a statement which is always true, or only mostly-always true?
In electrical engineering, a discipline I have studied, we have a similar rule, a logic signal is responded to as though it is either a high or a low.  However, in the middle are what are known as "metastable states," where the rules of thumb do not apply.  In fact, you can even theoretically lock up a logic circuit by presenting a steady stimulus in between two states.  Needless to say, designers of such circuits take great effort to ensure their logic is never exposed to such stimulus.
Do we have any evidence of neurons exhibiting behavior which defies the all-or-nothing law in some circumstances, or if not, what sorts of metastable behavior are seen when the stimulus is exceedingly close to that of the threshold?

If you only ask if it is always true or not, than here is the answer to your question: http://science.sciencemag.org/content/127/3296/468.short  Unfortunately, I don't know any other example as of now.

That article refers to a bundle of muscle fibers, not nerve cells. Muscle bundles don't exhibit all-or-nothing, or you'd never be able to pick up eggs. It's interesting because heart muscle is similar to nerve tissue in a couple of respects but the all-or-nothing law doesn't apply here.

@Resonating They are controlled via the same mechanism as nerve cells, namely action potential. The strength of contraction is determined by two things: the number of cells activated, and the frequency at which the action potentials are sent. Action potentials are of the same potential regardless of the contraction's strength.

I would argue the all-or-none principle is a rule of thumb. It is generally true if voltage hits a certain threshold then there will be a action potential with the same amplitude regardless the strength of the stimuli. But as you point out with the logic gate example, the threshold is notoriously hard to define mathematically. Furthermore Action Potentials don't always have the same amplitude, but as I will argue that doesn't matter all that much to the function of the neuron.
As most rules in biology we can find exceptions. I'll list some phenomena that confound the all or none principle.

Accommodation is the prime example that not all action potentials have the same voltage amplitude. Accommodation is the when the amplitude of the voltage of successive action potentials drops, and may even stop firing (Depolarization Block). This is usually the result of a too strong of a stimulating current, and occurs under pathological conditions.
Resonating Neurons These neurons fire when a certain frequency of input is achieved and can even fire when hyperpolarizing (negative) currents are injected. The reason I bring this particular neuron  type up is it shows that thresholds are not necessarily more depolarized (positive) than rest. They are complex manifolds (or shapes) relating to the gating variables of Ion channels in the membrane.

Another thing to note, is even though amplitudes of Action potential can change, the difference of a few millivolts in amplitude will not make a difference to the synapse and in that sense the all-or-none principle holds. Recall that voltage gated Calcium entry is required for a synapse to release it's neurotransmitter. Much like the logic gate, it will only enter at sufficiently depolarized (positive values) but the more positive the voltage, does not correspond to more Calcium entry. In other words it saturates at high voltages. In this way, to cause a stronger response at the synapse the neuron increases the firing frequency to stay "on average" depolarized longer. Thus more Calcium entry and thus more neurotransmitter release.


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What portion of America needs the Flu vaccine for herd immunity effects to become substantial?
I've been looking at the effectiveness of Flu vaccines, which are in my subjective opinion abysmal, and the concept of herd immunity.  I see many articles which argue that we all need flu shots to help support the weaker individuals via herd immunity.  However, I see very few documents actually indicating how effective this process is.
Most of what I have found on the topic is interested in the Herd Immunity Threshold (HIT), which appears to be the point where vaccinations drive the Rq of the disease (reproductive rate in the presence of the vaccinations) below 1 such that the disease spreads to fewer and fewer people with each generation, like removing the heat from a fire such that it cannot sustain itself.
There are two particular aspects of this which I believe are required to answer the question which I cannot seem to find a good answer for, which have been preventing me from answering my question:

What is R₀, the basic reproductive rate, for influenza?  I have seen estimates ranging from 1.2 to 3.  As best as I can tell, even a poor vaccine would be very effective if it was 1.2 but it seems like it would do very little against the higher R₀ values.
How substantial of a knee in the curve is there regarding the number of immunized individuals vs. the herd immunity effects?  If there is no substantial knee in the curve, that should indicate that there are valid herd immunity arguments for influenza even if the vaccines are substantially ineffective.  If the knee in the curve is sharp, then herd immunity arguments would only be valid if we could reach that threshold.

It appears some of these questions may have been answered in "The vaccination coverage required to establish herd immunity against influenza viruses" by PedroPlans-Rubió in 2012, but I do not have any access to Preventive Medicine, the journal it was published in.

The flu vaccine is a poor choice for this kind of analysis because of the tremendous number of variables involved: what was the dose inhaled/how intact is the 'victim's' immune system/how close is the match between the vaccine and the circulating (ever mutating) virus, etc. The world's epidemiologists struggle with this anew every year. The question is better for a virus like varicella.

@anongoodnurse True, it might be easier to analyze another virus, but influenza is the one I am interested in.  It is actually the variability and uncertainty surrounding influenza that draws my attention to it.  I see a great deal of certainty expressed regarding the influenza vaccine, but I'm having trouble finding numbers that back those certainties up.  For example, the anti-vaxers love to tout the ineffectiveness of the vaccine (perhaps 10% this year!), but I find it hard to find out what effectiveness is actually needed.  Maybe 10% is actually enough if we all do it!

I can't answer; the effectiveness changes every year. I can say, though, that as a young doctor, I recommended the vaccine but didn't get it. Four years in, I contracted influenza. I never missed a flu shot again, and never got the flu again (even though I treated such patients every year.) Decades passed. I contracted influenza again this year - only the second time in my life - in a year that the vaccine is a notoriously poor match. Maybe because I received the high-dose vaccine, my course was very mild. Others who have been immunized (chiefly infants) have died. How can you get hard facts?

Cort, you might want to look at the Cochrane Report. Keep in mind, though, that they don't only include influenza A&B (what the vaccine covers.)

Quoting Jhung et al. 2011 talking about H1N1 2009 epidemics

Although estimates of R0 from past pandemics vary, the R0 of previous pandemic influenza viruses generally range from 1.5 to 1.8 for the 1957 H2N2 and 1968 H3N2 pandemic viruses, and 1.8–2.4 for 1918 H1N1 influenza A strain, with a high estimate of 5.4 by Andreasen et al [see also White et al]. During the current pandemic, White et al used CDC case-based data from 1368 confirmed and probable cases with a date of report on or before 8 May 2009 and estimated the reproductive number of pH1N1 virus to be between 2.2 and 2.3. Estimates decreased to 1.7–1.8 after adjustment for increased case ascertainment during the initial pandemic period. In a sensitivity analysis making use of previous estimates of the mean serial interval, White et al estimated that the reproductive number was between 1.5 and 3.1. Fraser et al used data from the initial outbreak in Mexico to estimate R0 in the range of 1.2–1.6. Yang et al used reported case clusters in the United States to estimate R0 to be 1.3–1.7. Most estimates of R0 for pH1N1 virus, therefore, have indicated that the virus was at the low end of transmissibility, compared with the strains that caused the 1918 pandemic, and was comparable to or slightly less transmissible than the strains that caused the 1957 and 1968 pandemics.


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How fast do we fall asleep?
When looking at the process of sleeping, most research I find point to a group of mutually inhibitory cells which form a sort of biological "flip flop."  There's cells that promote awakenness and cells that promote sleeping.  The process we typically think of as "falling asleep" is getting to the point where this transition can occur, but I'm interested in the transition itself.
How fast is this transition? In engineering, we'll typically measure the speed of such a transition as a 10-90 measurement: the time it takes to go from a 10% signal to a 90% signal.  Is there a similar measurement made in such biological systems?

Good question. Please be aware that in biology, we are concerned with a subject with high variation. In other words, as you very well must know, the time needed to fall asleep varies very considerably between people and also within a single person, from day to day. I think the second paragraph in your question is counterproductive, I would edit it out to prevent answers going off at a tangent.

@SPr I'll have to think about how to best reword that second paragraph.  I put it in there because, when it comes to flip flops like this I know that it's a continuous process with no clear start an end, but the the duration of the middle of the flip is easier to quantify.

Our ability to maintain sleep or wakefulness is because of "mutual inhibition" between the wake-promoting neurons and the sleep-promoting neurons. The areas in brain which regulate wakefulness by activating the cortex also inhibit neurons present in ventrolateral preoptic nucleus (a cluster of neurons situated in the anterior hypothalamus). And when VLPO neurons are activated, they induce sleep, and this also inhibit activity in the arousal centers like neurons in tuberomammillary nucleus (TMN).
Transitions between these states of wakefulness and sleep is very rapid, usually in seconds. Various researchers have reported this neurological mechanism for "flip-flop switch" in form of electrical circuit.
The mechanism  for mutual inhibition is regulated by sleep drive or the circadian signal. When one of this body signal is sufficiently strong, it transits to the opposite state from wakefulness to sleep or vice versa. This mechanism is analogous to mechanism involved in  transition between rapid eye movement (REM) sleep and non-rapid eye movement (NREM) sleep.
Humans require some time to relax and then fall asleep, and deep sleep needs 20 or more minutes after sleep onset. Sleep onset and associated loss of consciousness is related to one another and occurs instantly.
Many intrinsic and extrinsic factors  regulate sleep cycle. Adenosine is one of the chemical which accumulates during wakefulness and later induces sleep by inhibiting wake-promoting neurons. And caffeine inhibits adenosine activity and helps in wakefulness.
The time needed for transitions between sleep and wakefulness  is  maintained by biological clock located in the suprachiasmatic nucleus. This is small structure consisting of about 50,000 brain cell. And it receives light signals from eye  via  optic nerve. Light controls the day-night cycle and which in turn regulates various biological functions including temperature, hormone release,  sleep and wakefulness. The SCN stimulates wakefulness by producing a  alert signal which inhibits sleep. The SCN also helps in inducing sleep by turning off alert signal.
(Via:  http://healthysleep.med.harvard.edu/healthy/science/how/neurophysiology)


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How does sunlight affect the longevity of SARS-CoV-2 on surface?
UV radiation is known to degrade most viruses rather quickly.  How does the UV radiation from sunlight affect the longevity of SARS-CoV-2 on surfaces.
Of particular interest to me is the virus' lifespan on gas pump handles, which are typically in covered but open spaces.

Please see here.

@David Thank you for the links, though they do not answer the question.  There was one FAQ question om the WHO which pointed out that UV light should not be used to sterilize skin, but that's because it irritates the skin rather than due to its effectiveness.  Another article from NIH points to it lasting hours-to-days on surfaces, but does not state any effect of UV.  I had seen both articles in doing research before posting, although I have to admit that was quite the nice collection of COVID-19 links!

I have no data on SARS-CoV-2 specifically, but for SARS-CoV UV radiation is an effective method of eliminating viral infectivity:

Irradiation of UV for 60 min on the virus in culture medium resulted in the destruction of viral infectivity at an undetectable level.
CONCLUSION: The survival ability of SARS coronavirus in human specimens and in environments seems to be relatively strong. Heating and UV irradiation can efficiently eliminate the viral infectivity.

Stability of SARS coronavirus in human specimens and environment and its sensitivity to heating and UV irradiation., Biomedical and Environmental Sciences (2003)

Yes, UV light is effective in killing all the viral and bacterial cells. And it is believed that UV-C  will be effective in disinfecting SARS-CoV2 which is responsible for Covid 19, as earlier it is reported that UV-C disinfection can degrade viruses which are similar to SARS-CoV2 virus (like SARS-CoV1 and MARS-CoV).
But, the effectiveness of UV disinfection is dependent upon exposure time and intensity. So, sunlight could not disinfect the gas pump handles which are not directly exposed to sunlight. Effect of heat due to sunlight is another factor which may be responsible to inhibit virus growth.
(Via: http://www.iuva.org/COVID-19)


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How do I measure genetic distance?
I'm not sure how to measure genetic distance. There seems to be many different equations out there, and all the ones I found are rather old.
In my specific problem I want to see if the twist in collagen differs if the species are different. (I have a program to predict collagen twist according to amino acid sequence)
I therefore want an objective numerical value to base my comparaison on. "Nei's standard genetic distance" seems good, but it is very old so I was wondering if there was a modern alternative. Is there an R package or something like that to calculate it automatically?

There are a few answers here, it is a little unclear which is closest to what you want.
[edited to be more complete and direct]
1) Nei's distance is mostly for comparing populations of the same species, so it should be fine if that is what you are doing. I am guessing that based on your post, you are more interested in cross-species comparisons. Of course, the logic is the same, it's just the math is different. For among-population divergence, Fst (fixation index) is also commonly used. But if you are using a sequence alignment or some such data to compute genetic distances, there are lots and lots of metrics. Some of them are very simple- for instance you could use Hamming distance and just count the number of residue differences between each sequence.
As for computing these metrics, there is a webserver called GenePop online that will compute Fst for you if you plug in a dataset. I don't know of R packages that compute these things, I would guess just by looking at wikipedia that coding functions to do this would be relatively trivial (if you are comfortable with r).
2) If you are truly looking among species, a somewhat more appropriate approach might be to model your species in a phylogeny, rather than to use distance methods (though the two are attempting to solve sort of the same problem). There are lots of easy-to-use online programs for this, for instance: FastML. You can just copy-and-paste a seq alignment in there. After you have the tree in for instance newick format, there are good tools for visualizing trees both online at iTOL, and through R with APE.
APE also has good utilities for modeling phylogenetic processes, so you could in principle directly model changes in protein folds through evolutionary time (assuming you have a meaningful summary of protein folding, either continuous or discrete).
I don't have enough reputation to link to more of the resources I mentioned, sorry.

I've already worked with SeaView for making phylogenetic trees but I am looking for a good numerical value I could use to do some data analysis (and very basic machine learning) Since time of divergence and simply counting different bases seemed a bit basic I am looking for something more accurate... I'm using amino acid sequences of collagen taken from PDB.  Thank you, your answer gives me a few pointers.

ah- i see. my naive guess is that all of the distance metrics will tell you similar things. nonetheless, since you are working with different species and want a more sophisticated distance metric, you might try something like protdist from [phylip] (http://evolution.genetics.washington.edu/phylip/doc/protdist.html), which has various substitution models available. Again, I would recommend trying to model the problem phylogenetically, which is preferred in the field. Distances can be tricky because observations are non-independent. But probably most methods will give the same. Good luck!

I think my approach would be to make a phylogenetic tree and color the tips by collagen twist. There are several R packages to help with this, including APE, ADE4, and poppr. To make a phylogenetic tree, you first calculate a distance. You mentioned Nei's, and that's actually still used pretty commmonly. I know you're not doing population genetics, but check out this tutorial: https://grunwaldlab.github.io/Population_Genetics_in_R/Pop_Structure.html. They calculate Gst (mentioned in the other comment), talk about a few different distant metrics (including Nei's), make phylogenetic trees, and it's all in R. They even color the tips by population - in you're case, your populations would be types of collagen twist with your samples named by species (Lizard-1, Lizard-2, Chimp-1, Chimp-2, etc.). You also could color the tips by species and name your samples by twist type (forward-1, forward-2, reverse-2, etc.). I know this question is old, but hopefully someone else who stumbles here will find this answer helpful.