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What made this small light weight bee hive-like structure?
This structure was photographed in mid December in Eastern Iowa, USA along a path within a public use area with tall grasses framed by small to medium trees.  It is approximately 5 cm (2 inches) long and 10 cm (4 inches) in diameter.  It had the light airy appearance of honeycomb but was one solid ribbed structure attached to a small branch.  I'm not sure if this was something used over the summer by an insect or if something will come out of it in the spring - winter temperatures often go below -18 degrees C (0 degrees F) in this area of the country.  Any help would be appreciated.

This is a mantis (Mantodea) egg sack, or ootheca. The female mantis makes it in the fall and it will remain over winter until (juvenile) nymph mantises emerge from it in the spring.
The following site introduces how to raise mantises from eggs but also has some general background information including on how seasonal temperature changes can affect the ootheca:
https://www.keepinginsects.com/praying-mantis/caring-for-mantis-eggs/


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What is this insect from Brazil

Im assuming 'cicada' with this insect but which one ? Small size- c1c-2 cm -

A better assumption would be "planthopper" (superfamily Fulgoroidea), but beyond that I admit to not having a guess.

I think you're right ....

source: Stack Exchange

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sort: votes


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ID this insect please. SE Brazil Oct 2017

A number of these large flies were praying on smaller stuff / mid day / in the low altitude rainforest sections of SE Brazilian Rainforest

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I would like to know what this insect is please

Noted on the side of a tree in the Brazilian Atlantic Rainforest in Oct 2017. About 3-4 cm long . Middle of a very hot day.

That is a planthopper, order Hemiptera, suborder Auchenorhycha, Superfamily Fulgoroidea. It looks to be in the Genus Phrictus. Very similar to a picture I saw on the web of Phrictus diadema.


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ID please.Small insect from Brazil

Photographed in south east Brazil in the Atlantic rainforest during October 2017


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Is there an existing database of mutation rates for mitochondrial loci?
I'm wondering if there exists a database of mutation rates (transitions and transversions) for both mitochondrial loci (such as cytochrome c oxidase subunit I (COI)).
Due to the use of COI as a DNA barcode to identify animal species, this gene has a relatively high mutation rate despite being quite conserved across major taxonomic groups. Thus, substitutions in COI are expected to become diagnostic of species much more rapidly (also because of the 4-fold lower effective population size compared to nuclear markers).
The reason I ask is because I am developing a simulation algorithm allowing a user to generate random DNA sequences under a specified nucleotide evolution model (e.g., Jukes-Cantor, Kimura-2-Parameter). I would like to be able to specify realistic mutation rates of transitions and transversions in order to closely mirror actual substitution rates in COI.
Any insight would be much appreciated

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Island model vs. stepping stone model
Wright's Island model and Kimura's stepping stone model are classic explanations for migration/gene flow o individuals between subpopulations within the field of population genetics.
My question concerns the quantity Nm, the (effective) number of migrants per generation.
In the Island model, where all demes are exchanging migrants at a given time, individuals migrate with a frequency of m, as seen in Wright's approximation for $F_{ST}$
$F_{ST} = \frac{1}{4Nm + 1}$
In Kimura's stepping stone model, individuals can only migrate to an immediately neighbouring subpopulation with a frequency of $\frac{m}{2}$.
My question is:
In the stepping stone model, are there still only $Nm$ individuals migrating, or is it now $\frac{Nm}{2}$?
My thinking is that an individual can either move left or right, each with a frequency of $\frac{m}{2}$, for a total of $\frac{m}{2}$ + $\frac{m}{2}$ = $m$, so that there are still $Nm$ total migrants. Am I correct in my thinking or should it really be  $\frac{Nm}{2}$?

It all depends upon how $m$ is defined and that might vary from a paper to another.

I thought that may be the case. Was SimBit designed assuming $Nm$ or $\frac{Nm}{2}$?

It all depends upon how $m$ is defined and that might vary from a paper to another. The rest, I find, is very much just a question of logic.
In the infinite island model (the model from which Wright's approximation was computed), the total number of migrants is of course, infinite (if $m≠0$). With $d$ demes (or islands), the total number of migrants is $dNm$ if $m$ is defined as the migration rate between any two patches.
Under a linear stepping stone model with only 1 step (because there exist more complex stepping stones models), with $d$ demes (or stones), the total number of migrants is $dNm$ (minus small approximation for the extremities of the world) if $m$ is defined as the migration rate from one deme to an adjacent deme. Half of $dNm$ are migrating toward the left and half of them are migrating toward the right.

I thought that may be the case. Was SimBit designed assuming NmNm or Nm2Nm2?

In SimBit, you can use multiple modes to enter migration information. You can specify the migration rate from any patch to any other patch (mode A).
You can use island where you specify the probability of not migrating (which might arguably be a little unintuitive). If the probability of not migrating is $x$, and there are $d$ demes, then the number of migrants from one deme which patch size is $N$ to a single other deme of interest is $\frac{N(1-x)}{d}$. The number of migrants from this deme to any other deme is $N(1-x)$ and the total number of migrants in the whole (meta)population is $dN(1-x)$.
The mode LSS (Linear Stepping Stone), is a little complex as it is very flexible. You can specify the migration rate from a focal patch to any other patch considering they are place in a linear order. SimBit LSS indeed allows for stepping several stones apart if you want. If for example you input LSS 3 0.1 0.8 0.1 2 it means that the probably to migrate from any patch to a given adjacent patch is 0.1. The probability of migrating is 0.2 and the probability of not migrating is 0.8. With such model, the number of individuals exiting a given patch is $0.2N$ ($0.1N$ on each side) for a patch of size $N$. Assuming all patches have the same size, the total number of migrants for a (meta)population of $d$ patches is $0.2dN$.
Of course, if you allow for patch size to vary with carrying capacity or for migration rate to be affected by population mean fitness, then this expected number of migrants will vary among generations.


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How many polynucleotides are there in one molecule of DNA?
I always thought that a molecule of DNA was made of two polynucleotides each making up one strand of the molecule... Is that right?

No, you're wrong. One molecule of DNA is made of two polynucleotides. You should have a look at this: https://biology.stackexchange.com/questions/66343/is-a-dna-molecule-a-single-strand-of-polynucleotide-or-two-of-them-linked-togeth .

@MartinKlvana Being more assertive, stating i have given you the right answer or making an argument from authority by appealing to your experience is not how you convince anyone of anything. On the other hand, Mark pointed to a post offering evidence of authors clearly defining a molecule of DNA as being made of two strands. If you disagree with this terminology and think that most authors use the term differently , please respectfully suggest your own answer at the linked post.

@Mark This post seems to contradict your claim would be better than No, you're wrong. Martinklvana would probably had reacted differently if your opposition was made in less absolute terms. Note that when dealing with questions of terminology, it is better not go into absolute certainty as different authors may use the same word differently.

The term molecule was coined by chemists to describe small entities in which the atoms are joined by covalent bonds. When one is talking about large biological entities involving non-covalent bonds (proteins, nucleic acids) the strict definition often conflicts with the way one conceptualizes these entities, and this has led to common usage that may strictly be regarded as incorrect. However the definition of a molecule is of no real concern to molecular biologists and few people care that the situation is ambiguous.
Definition of Molecule (Wikipedia)

A molecule is an electrically neutral group of two or more atoms held together by chemical bonds

By this definition double-stranded DNA consists of two molecules, and haemoglobin consists of four molecules (or perhaps eight, if one regards the haem as a separate molecule).
Use of Molecule to refer to multistrand Nucleic Acids and Proteins
Because we are often concerned with the functions of a double-stranded nucleic acid or a multi-subunit protein in its entirety, one finds them referred to as molecules by quite reputable sources. For example:
Encyclopedia Britannica

Each hemoglobin molecule is made up of four heme groups surrounding a globin group, forming a tetrahedral structure.

Protein Data Bank: Molecule of the Month

DNA is arguably one of the most beautiful molecules in living cells. Its graceful helix is pleasing to the eye. DNA is also one of the most familiar molecules, the central icon of molecular biology, easily recognized by everyone.

Conclusion
It would be better to spend one’s energies on more important and intellectually interesting topics concerning nucleic acids and proteins then whether only their individual strands or subunits are truly molecules.

In general, it is right since with the term DNA you commonly refer to the double-stranded DNA. However, you need to be aware that DNA may exist in different forms.
Single-stranded DNA (ssDNA), for example, is composed of only one strand of DNA, so one chain of nucleotides or one polynucleotide molecule.
Double-stranded DNA (dsDNA) is the common form of DNA found in cells and it is composed of two polynucleotide molecules.
Triple-stranded DNA (tsDNA ?) also exist, which of course, is composed of 3 polynucleotide molecules.


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How many nucleic acids is there in "one molecule of DNA"?
I am confused...  People usually say that "DNA" is made of two strands deoxyribonucleic acid bound together. Nonetheless, the acronym "DNA" means "deoxyribonucleic acid".
So by logic, a molecule of "DNA" should be only made of one strand of deoxyribonucleic acid, and not two! Right?
This is really confusing...

DNA as we think of it is double stranded in its native (normal) state, so when we say "a molecule of DNA" we mean the standard, double stranded helix found in our cells. DNA is unstable as a single stranded molecule, so when saying "one molecule of DNA" it refers to the double stranded helix that DNA forms as this is the most common stable form. :)

Ok... So  "one molecule of DNA" is made of two deoxyribonucleic acids, right? Even though "DNA" is an acronym for deoxyribonucleic acid, the number of deoxyribonucleic acids that makes up "one molecule of DNA" is not specified when saying the word "DNA". Am I correct on that?

Yes. "One molecule of DNA" encompasses 2 strands in a double helix shape.

You are thinking about a nucleotide (A, C, G, or T). Nucleotides are molecules, and are the building blocks of DNA. DNA is synthesized from existing copies (not de novo), so there is always one strand, from which nucleotides are added to in a 3'-5' direction.


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Is a single polynucleotide necessarily and always a nucleic acid?
I am confused. I know that a DNA molecule is made of two polynucleotides.
But does each polynucleotide represent one nucleic acid? If so, a DNA molecule is made of two nucleic acids, right?
Or do the two polynucleotides (that form a molecule of DNA) make up only one nucleic acid? If so, a DNA molecule is only made of one nucleic acid, right?

What do you mean by "two polynucleotides"? I would say "two polynucleotide strands" - start with a nucleotide, connect some of them together and you have a nucleic acid (strand), join two of those and you get double-stranded DNA. Is this not covered in wikipedia pages like : https://en.wikipedia.org/wiki/Nucleic_acid ?

Well, each strand of a DNA molecule makes up one polynucleotide... Right?

I would just say it "is" a polynucleotide, but yes - double stranded DNA is two polynucleotide strands wrapped into a helix.

See that's the problem... You're talking about "polynucleotide strands". But how many polynucleotides is there in one strand of DNA: a) one b) many?

One. A polynucleotide is made of multiple nucleotides - it is a strand.

Oh ok. So, there are two types of nucleic acids: 1) DNA --> which is double-stranded, so it's made of only two polynucleotides 2) RNA --> which is single-stranded so it's made of only one polynucleotide. So if we get back to my original question "Is a single polynucleotide necessarily and always a nucleic acid?" --> the answer is no, for DNA is a nucleic acid and it is made of two polynucleotides. Am I right?

Yes, that's right.

Hallelujah! I finally understand! Thanks a lot, man!!

Possible duplicate of Is a DNA molecule a single strand of polynucleotide or two of them linked together?

I would advise you to focus on ideas in molecular biology rather than questions of nomenclature, which betray a chemical attitude to the topic. Counting strands is not where the action is, but if you do so at least get it right.

There are two types of nucleic acids: 1) DNA --> which is double-stranded, so it's made of only two polynucleotides 2) RNA --> which is single-stranded so it's made of only one polynucleotide. So if we get back to my original question "Is a single polynucleotide necessarily and always a nucleic acid?" --> the answer is no, for DNA is a nucleic acid and it is made of two polynucleotides.

...and some RNA viruses are double-stranded. As I commented previously, I suggest you stop counting the strands in nucleic acids and study their biology.

Your question arrangement is wrong, DNA is made up of 2 polynucleotide strand indeed. And these polynucleotides are the polymers of nucleotides, where nucleotides consist of deoxyribose sugar in case of DNA and ribose sugar in case of RNA+nitrogenous base+phosphate. Yes it is always a nucleic acid.


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Is there enough vitamin B12 in lakes, rivers and ponds, for humans not to need to take supplements?
Vegans will often say that having an animal-free diet is best for our health and is actually the diet that humans should be eating to function optimally. To which meat eaters will raise the issue of B12, and how (they believe) it is only to be found in animal products [thus vouching for an evolutionary need to eat meat and eggs). These days, with all our water being treated to remove pathogens, it is obviously best to take b12 supplements, but the question remains: do vegans have a point? Is there actually enough b12 in water for humans to not develop an insufficiency?

I was not aware that drinking water was a source of B12 at all! It might be clearer to start with that information, and then ask whether the source is sufficient.

Even if it was the case that B-12 could be absorbed from water-borne microorganisms, 1) Wouldn't it depend on the particular body of water you drink from, e.g. a stagnant pond vs a spring-fed mountain stream? 2) Before water treatment, weren't water-born microorganisms a major source of diseases such as cholera?

@jamesqf It would certainly depend on the source I think. Obviously, stagnant water with more algae, particularly in lakes would contain more B12 than a mountain spring.  I was concerned about cholera, but cholera and many other such diseases are the results of non-nomadic living. City environments, where waste is allowed to build up, cause widespread epidemics. My question is in terms of human history, before the advent of agriculture and settler communities.

Of course there is no evidence for the superiority of the vegan diet claim to begin with, so there is that, and there are plenty of vegan foods fortified with B12, even some from non-animal sources.
No, there is not enough B12 in treated water nor well water for a human. There can be enough B12 in untreated river/lake water because it contains high levels of fecal matter or algae which is high in B12 (b12 is manufactured by anaerobes).  Of course these are the things you want removed from your drinking water so reducing B12 is inevitable. Also can contain enough being the key phrase it depends on the water source, cleaner river contain less.
Evolutionarily speaking humans eat animals for the same reason every omnivore and many herbivores (deer, ect) do, because we can, it is generally a superior nutritional substrate which is more than enough for evolution to favor it.
source 1
Source 2
source 3

Could you elaborate on your definition of 'superior'? I said vegan diets were healthier not 'superior'. @John

which there is no evidence for. And by superior substrate I mean easier to digest, more calories, more vitamins, an animals contains everything you need since it is basically made of the same stuff.

No evidence? https://www.youtube.com/watch?v=30gEiweaAVQ

@Samuel   Vegetarian not the same as vegan diet, it is a pretty important distinction.

The video compares research from 3 primary groups, meat eaters, vegetarians, and vegans, on most points.

It is also a video put out by one individual trying to sell something, an actual source would be important. It is basically one long string of cherry picked data and conclusions out of context. Sourcing requires more than just flashing the headline of a paper for a few seconds. Gregor is a known for exagerated and unfounded claims and the video has been debunked before, https://sciencebasedmedicine.org/death-as-a-foodborne-illness-curable-by-veganism/. Worse many of his claims are outright lies counter to the papers included actual conclusions, the video is pure propaganda.

Fermented food is a safer and higher b12 option for a vegan, it can have a lot higher content of yeasts and bacteria than safe water, and it can be controlled.
Most vegan foods (not protein rich) can safely ferment until 50% to 99%(sry for the humor) of their expiration date, living plant matter in any carb/plant mix will generally kick off a good fermentation. some foods like salad couscous are full of yeast and become unappetizing and gluey with yeast a long time before they become unhealthy to eat.
It would be difficult to design a pond/lake which has high content of bacteria and archea and chlorella to be optimal for humans, whilst also being safe for children. Rivers should have mats of algea that filter the water, however they are so variable, it's pot luck if a river has an excess of nitrogen or a silty bacterial nuisance, A river can be jam packed with nitrogen detritus, and after a storm/ in the wrong place it's not reliable.
In winter the lake can become less productive biologically, too high in nitrogen, and if it's biologically rich it will be subject to wild seasonal variability.
Blooms of animals, daphnia, cyclops can occur, eating whatever is making the vitamin b12, and any unseen bacteria can bloom, which benefit from warmth and that will thrive noxiously in the gut.
A snail doesn't even have a lot more neurons than a tardigrade, and definitely a lot less neurons than small insects and acarians that you accidentally consume from plants.
You can reprimand me for the lack of references, it will give be a subject of study, however it's too broad a topic to reference and research right now, unless you think i've made an overstatement.


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Does donating blood lower testosterone levels?
I'm a guy and I decided to donate blood because of persuasion. My testicles feel weak afterwards specifically. I mean they feel like they're compensating -- assuming that makes sense.
Is this because significant blood volume loss would affect testosterone? Are the testes working harder to produce testosterone after a loss of so much blood from the body?
I also feel a little weaker overall as well, but the question focuses on testosterone. Clarification?

No, on the contrary donating blood increases testosterone levels in blood.
Testosterone actually decreases the level of the iron-regulatory hormone; hepcidin, allowing for more iron to be absorbed from foods. This is one of the reasons why men tend to have higher hemoglobin levels and larger blood volume than women do but over the time excessive amounts of iron in body can suppress the function of the hypothalamus, pituitary gland, and testicular leydig- and sertoli-cells, resulting in lowered testosterone levels. Donating blood reduces excess iron build in men and boost testosterone level in blood.
Sometimes people who donate blood notice a few minor side effects like weakness, nausea, light-headedness, dizziness, or fainting, but these symptoms usually go away quickly. These symptoms occur because the donor's body usually replaces the liquid part of blood (plasma) within 72 hours after giving blood. It generally takes about 4–8 weeks to regenerate the red blood cells lost during a blood donation.
References
http://knowledgeofhealth.com/to-boost-testosterone-maybe-donate-blood/
https://www.anabolicmen.com/iron-and-testosterone/


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Reference request - Neuroscience of Free Will
I am a computer science student taking a course on philosophy. My topic of research is on freedom of will and whether it is possible to create a machine capable (or closely) of doing so.
I felt that my first steps would be to find some articles related to the brain, to find out which part of the brain is fully / partially responsible free will, the activity that goes on in the brain when one is 'exercising his freedom of will'. I have been searching on google with keywords like 'free-will, neuroscience, brain' but have not found a good article.
I was hoping for the community to give me some nice references for a good start. Anything related would be kindly appreciated as well.

I'm sorry to say this question is likely outside our guidelines for a number of reasons. I recommend reading through the asking guidlines and the help center in general and then seeing if you can formulate a question that's more within the scope of this site.

You need to choose your definition of free will. Under the incompatibilist's view you are out of luck. Under the compatibilist's approach, the issue simply boils down to decision making, of which several computational models exist. Under a strict definition of free will, you must accept some source of causation other than physical determinism, something that is not compatible with the scientific approach. So, you'll either have to relax your definition or reject its existence.

You seem to be assuming that free will occurs at all in the universe.

You might want to search for publications by Felix Tretter (most are in German, unfortunately)

I'm voting to close this question as off-topic because ‘free will’ is a philosophic not a biological concept.

One potential argument has been introduced in an essay of the biologist Martin Heisenberg, and relates to the stochasticity of chemical reactions that occur within biology.
Note that, depending on the philosophic tradition, this may not be regarded as free will.
For a link to the original essay (paywall), and the follow-up comments (and objections) by other scientists - of which all appeared in the reputable journal of Nature - see: https://www.ncbi.nlm.nih.gov/pubmed/19444190


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Database for Macroinvertebrate Taxonomy
I compiled different data sets of invertebrate occurrences across some countries and now I want to ensure that all the taxonomic information is homogenized and correct. To this end, I am looking for a database which allows me to evaluate my date. Basically, the equivalent to what algaebase.org is for algae.
I know about gbif.org but already found some mistakes in there.

Have you sent your observations to gbif.org? Sure they would be happy to improve their database...

No, not yet but thanks for the suggestions I will consider it in the future.

So, you have the mistakes you found, why not send those now?

Because I did not keep a record. I just cross-checked algae base with gbif on some species and found different results on what is considered the expected name and what a synonym.

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Are humans known to be "poisonous" to any animal?
Are there examples of non-herbivorous animals that could be poisoned if they feed on humans because of the composition of our bodies/blood?

Human is not in the menu of other animals (in normal circumstances) and there aren't any studies regarding to this (as you can guess) so we don't know if human meat is toxic to any other animal. There are instances where other animals ate human though (for example: great white sharks and lions). On the other hand,  cannibalism can lead to a disease called Kuru which is caused by abnormally folded prion proteins. Thus, we could say human meat is toxic for humans.

Hmm, this "non-science related" book claims that: "Human meat can be poisonous for protected species like crocodiles."


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Methane and wetlands
Some papers I have read show carbon accumulation (peat) in wetlands is reduced because of low methane emissions. Why is this the case?
Why does low methane emission reduce carbon accumulation in wetlands?

Welcome to Biology.SE! Could you provide the links to the papers you read?


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Can intracellular protein initiate strong immune response?
Some autoantibodies escape immune tolerance and can cause autoimmune disease. In order to cause harm to the tissues by these autoantibodies, do the antigen need to be extracellular or membrane bound, so that they are exposed to the immune system?
What happens if the target protein of the autoantibody is intracellular? Does the cellular localization of the target antigen plays any role?


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Metatranscriptomics Extraction
I am attempting to perform metatranscriptomics analysis of a cleanroom. The DNA input is known to be rather low (<1pg). Despite this, I want to still attempt to try it. I am thinking it might be best to perform extraction trials before hand where certain parameters are manipulated. I can then determine from these extraction trials which values for which parameters are best.
As an example, I am reading a peer-reviewed paper called "Validation of picogram- and femtogram-input DNA libraries for microscale metagenomics" where they used the Illumina Nextera XT DNA library preparation kit on low biomass samples. Two of the parameters they manipulated were:
1) PCR cycle numbers (Values = 12, 14, 16, 18, 20)
2) ATM dilution (Values = undiluted, 1:5, 1:10, 1:20, 1:50)
I am hoping to use the same type of extraction trials to determine which combination of values from these two parameters is best for a clean room. My first question is: How can I determine which combination is best (as there are 25 combinations)? I have two ideas (but am open to others):
1) Check the amount of RNA derived
2) Check some quality metric on RNA
As I hope to do triplets of each of the 25 combinations, I will have 75 samples. I am hoping not to have to do sequencing as it is time consuming and possibly expensive in order to chose the best combination. Is there a way to chose which combination works best without having to sequence?
My second question is: Are there any other parameters in this workflow that I can also test for if I am not getting decent results in these low-biomass cleanrooms?
(As you can tell, I do not have too much direct molecular biology experience, so feel free to correct or question any of my post and/or "dumb down" your response). Thank you for sharing advice (for either question)!

Consider doing triplicates of just 4 combinations of cycle/dilution: low+low, low+high, high+ low, high+high.  Simpler.
Most important: prove you can extract DNA from a clean room.  If you extract from a real clean room and get no result from the PCR, maybe it is because you failed to collect anything or maybe nothing was there.   Idea - spray a known quantity of DNA into a room that will serve as your sham clean room.  Then do your extraction protocol.  You can test the cycle / dilution parameters with the sham clean room extraction and have those variables optimized for when you collect from a real "wild" clean room you did not dope with DNA.


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Is my Y-chromosome the same at 78 as it was at 18?
How accurate is a Y-dna test at age 78?

By and large, yes.  Some telomeres might be shorter, but the rest of the sequence will not change.  Certainly, any regions used for ancestry testing will be stable.


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Can cognitive functioning of the human brain change the physical state of the brain?
Can cognitive functioning of the human brain change the physical state of the brain? E.g. does self-awareness, self-reflection change the number of neurons or synapses among neurons? I.e. I am trying to develop self-modifying neural networks as described in my other question https://ai.stackexchange.com/questions/7966/dynamic-self-improving-self-modifying-neural-networks-which-can-simulate-goede and I am interested in the biological process that can be analogues of self-modifying neural networks. What determines the physical structure of the brain - number of neurons and synapses and are the cognitive functions among the determinants? I guess that generally the brains can be less developed matter comparing to the artificial neural networks that humans can invent or that can self-evolve in silica after sufficient period of time and that is why human brain can be more restricted in its self-improving capabilities than in silica ANNetworks. Similar situation is with genetic algorithms which can allow unrestricted number of sexes while biology has at most two sexes.

Your question has loads of unjustified assumptions.

There might be an answerable question buried in here (the title question is somewhat answerable), but it is obfuscated with a bunch of other conjecture that is unsupported and not helpful towards clarifying your question. If your interest is just in ANN, you should stick to ANN and understand that the connections with biology are analogies. If you want to learn about biological neural networks, you should start with a more basic understanding of neuroscience first.

One can invent lot of features for ANN, but I just wanted to be sure if there are analogies with biological world. Although I am not sure about value of such analogies, maybe existence of them gives some reputation to ideas and gives hint that this is path worth exploring.

@TomR Bryan is right; interesting though the metaphor is, the more you learn about machine learning and neuroscience, the more you realise the comparison is almost useless.

Also agree with @BryanKrause. Here is a link to a related answer of mine, although it deals with the case of a single biological neuron at the phenomenological level.

@TomR Biological networks can be motivation for trying new tricks in ANN, but the cost functions are very different for biology versus silica. Some computationally intensive artificial computations are done effortlessly in biology, and some biologically implausible approaches work great in ANN. We're far enough into understanding both that they have diverged: if you want to make a better ANN, study ANN. If you want to learn about biological neural networks, study biology.


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Computational approaches for making hypotheses about the effects of genetic engineering? Experiment planning methods?
Let's assume that I am searching for gene editing candidates for curing human adiposis. Are there computational frameworks that can allow me to select the best candidate-genes for editing via some CRISPR-like tools? I guess, that extensive databases of already performed experiments are available and human mind is required to select candidate genes for experiments. But maybe there are some methods, that allow computational select, planning of experiment, e.g. using: 1) already known biological pathways for different biological processes or incomplete pathways for the process under consideration; 2) protein-protein interaction models to predict some pathways and to select genes from them. Etc.
I am complete novice for this field, coming from computer science and only starting to read books about molecular cell biology, epigenetics and protein-protein interaction. Maybe there are special terms that allow me to Google for the subject of this question

I suspect that what you are asking for is years in the future yet. Bear in mind that the use of CRISPR-CAS9 is just entering clinical trials for a very few, well studied diseases. Almost all the work with CRISPR-CAS9 is still limited to model organisms and tissue cultures.
Are you referring to Adiposis Dolorosa?  Apparently the cause is not actually known yet. It's thought to be heritable, but it isn't known to be associated with a single gene or family of genes. The most common technique for analyzing what genes and gene mutations cause disease is Genome Wide Association Studies (GWAS), so you might use that as a staring point for your searches.
There are several computer programs that try to model what pathological effects a given mutation will have, but these are pure research at this point, and typically require extensive training for each gene or protein product. Try searching for "sequence based pathology prediction". However you may not find much related to Adiposis Dolorosa since the causative genes are apparently not known yet.


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Why are human wastes yellow?
Except for the feces, which is more brownish, all the human wastes (urine, earwax, snivel, phlegm, and rheum) are usually yellowish. Why is that?
I heard that urine is yellow due to bilirubin(?). What about others?

It is because of the pigment stercobiline which is present in human faeces

If your phlegm &c are yellow, you probably have a respiratory infection.


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Is it possible to discriminate tetrachromacy using sRGB color?
Hi I'm a physics grad student who has lots of interest on color perception.
I have recently learned that some people (mostly women) have another active cone cell which makes them possible to discriminate more colors than usual people like me.
Is it possible to discriminate tetrachromacy using sRGB color, I mean, is it possible to test it out on computer monitor? I guess so, because even though computer use combination of only 3 colors, it seems possible to make 2 combinations different in which is only perceptible to tetrachromacy. However, I'm not sure about that point because I'm not expert on that.
Anyway, if I'm right, it would not be so hard to make a test which resembles dyschromatopsia test, that can distinguish trichromacy and tetrachromacy. I couldn't find such a thing on internet. Test I could find seemed not valid. Even I could pass all the tests, but I'm not clearly tetrachromatic person.
Can somebody help me?

All the combinations of three sRGB primary colors are distinct for a trichromat. This immediately precludes any way to find out whether you are capable of more: if even a trichromat can distinguish all the colors, tetrachromat even more so.
But in principle, three colors are sufficient to check for tetrachromacy, but they can't be the sRGB primaries. The three colors you need must lie on one line on the chromaticity diagram, so that multiple mixtures of them could appear as the same color to a trichromat. Then a tetrachromat may be able to distinguish the two mixtures, which are metamers to a trichromat.


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replenishment of wild salmon
I understand fish from salmon farms are inferior, so I am wondering if it would be better to 'seed' the original waterways with wild caught roe/milt?  I am sure it is complicated, but so is salmon farming!

What do you mean by "inferior"? Also, once the claim is clarified, can back it up with a reference (and make phrase it as a hypothetical scenario)?

The process you propose is called 'stocking', and has been carried out for many different fish species for many years. The practice is, as you suggest, complicated, and more than a little contentious.
In the specific case of Atlantic salmon, Young et al. (2014) provide a non-technical overview of the conservation, population-genetic, and infectious-disease factors at play in stocking decisions. In general, fish raised in hatcheries are often wild-caught, which decreases the wild population, and once they are released, they sometimes have lower survival rates and reproductive success than truly-wild fish. If fish are raised in captivity for multiple generations, they can show evolutionary adaptations for captivity, and once released, captive-adapted fish can introduce harmful genes to the wild population. Similarly, captive-reared fish may be at an increased risk of communicable disease, and may introduce diseases to wild fish after their release.
A further complication from stocking is the impact of the stocked species on the local ecosystem. Many commonly-stocked species are non-native in the areas where they are released, and have negative impacts on the native species in that area. For example, brown trout have been introduced to many waterways in New Zealand, and they are predators of many native species, and compete for food with others. The New Zealand government has trialled an eradication of brown trout from some high-value conservation waterways in order to minimise the ecological damage caused by trout.


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Please help me identify this jelly fish
I've seen these jellyfish in thailand and was wondering what species they were. All I know is that there are lot in the Chonburi area and they sting in not deadly but hurts.
Images for the jellyfish
Thanks for the help!

Those pictures don’t look like a complete jellyfish, which makes identification very hard. Also, there’s no sense of scale in the pictures - can you describe them in more detail since you were there to see them personally?

Well the bigger ones are around 15-25 cm tall (in water the ones I could see at least) and around 10-15 in diameter. I don't know if they are complete or not I could only see there are also one smaller which was around 10cm in height and 5 in diameter with a similar structure. Well they are hardly noticeable in water because the water is not too clean so I couldn't take picture in the water.  Also there are some people eating them on the shore. And their sting also leaves red lines like other jellyfish sting and usually hurts for around 15 minutes (asked others who were sting before)

It looks like a Rhizostomae, or crown jellyfish, but it's hard to tell. The  article here does mention that it's edible though and it's found in Thailand so I'm pretty happy with that guess.
More specifically, it looks similar to the jellyfish asked about here, which was eventually classified as a Lobonemoides, perhaps Lobonemoides robusta


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Why are these ants moving as a pack?
Recently I took this shot of a 'pack' of ants moving towards some destination, and I was wondering, is this normal? Aren't ant scouts lone wolfs, and when a viable source of food is found near the ant colony, the worker ants form a trail to facilitate transport? If so(I'm poorly versed with biology as such, being an electrical engineering student), what purpose could this formation serve, my opinion being bent on supposed predator protection. This is not the only one I've noticed, but it is new to me, and a quick google search without any technical terms to feed it, yielded nothing substantial. This is the monsoon season here in India, if it is of any consequence to this peculiar behaviour.
I'd love to found out more about this(tag edits would be helpful), thank you :D

As you are engineering inclined, I would suggest you look at the Ant colonization optimization algorithm. This optimization algorithm is based for the most part on "real-life" ant behaviors and uses as a premise the pheromone-based communication of ants.

This looks interesting! @cagliari2005

This is a really wonderful phenomenon. Ants disperse far and wide, but when one of them finds food, it brings it back to the nest, and in doing so leaves a pheromone trail. The next scout follows this trail, and finds the food, and then leaves a second pheromone trail over the first one. As this continues, the trail gets stronger and recruits new ants to haul off the bounty. You can have fun with this. Take your finger and rub across the trail to erase it. Or place a piece of tape over it. This will confuse the ants for a while, until they make a new pheromone trail. If you have some time, break up a potato chip, or some other bait, and put it on the cement. Watch the first scout find it, and then leave a trail behind. Soon there will be many.

Sir if I'm understanding this correctly, this is the beginning of a food trail with an initial number of ants joining it, and more would do the same eventually. I did consider this, but what was odd was that, for one, the ants were in no hurry to scuttle back, i.e. they were walking at an extremely leisurely pace, waiting for the group to reassemble, and then moving, and secondly, the fact that they were moving in a single direction barring a few ants which look like they are straying off course, but not going in the exact opposite direction as would the case with a pheromone trail be.

They are not in a hurry. You are correct that in a food trail, you would eventually see ants going in both directions. They may be moving away from the nest in a single line, and then dispersing later to search for food.


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What is the name of this spider and is it poisonous?

We found it between Palm trees in the backyard of a home in West Palm Beach Florida.

Ah, that would be the spiny orb weaver. You can see an almost exact same picture here. To make a guess on the species, its maybe Gasteracantha cancriformis as its said in that webpage I have tagged. They are generally harmless. Here's the wikipedia page.


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What is the name of the bug that emerging from a wood chip like cocoon?
We found it on the wall of a home at West Palm Beach Florida. Is this a kind of infestation or a sick tree near the house fall on the wall?

That is a bagworm moth, in the family Psychidae. https://en.wikipedia.org/wiki/Bagworm_moth


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Large nocturnal butterfly with red and black hindwings
Location:
Central Poland, urban environment.
Size:
Around 4 centimeters long.
Time:
Early July.
Images:

That is a moth, in the family Erebidae. It is in the genus Catocala. Wikipedia has a nice page on Lepidoptera of Poland. https://en.wikipedia.org/wiki/List_of_Lepidoptera_of_Poland
including all the Catocala there.

It looks a lot like Catocala elocata.


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Flow cytometric counting of apoptotic adhering cells
I have been trying to measure rates of apoptosis in epithelial cells by marking apoptotic cells with annexin V conjugated with phycoerythrin (PE) and sorting using flow cytometry. Unfortunately, the cells are adherent, and have been cultured in a collagen coated plate. Thus, to suspend them for flow cytometry, I have been using a trypsin treatment. Unfortunately, my results have been quite poor. I believe that there are several problems. First, the trypsin treatment is likely to induce the disruption of integral membrane proteins, potentially causing the externalization of phosphatidylserine (PS) (to which the annexin binds) on the outer plasma membrane of cells. Since the cells were incubated with the annexin V following suspension with trypsin, this could have led to a substantial increase in apparent rates of apoptosis, and masked real differences between rates of apoptosis in WT and KO cells. Furthermore, I was informed that epithelial cells, in order to maintain their structural integrity, have a relatively large ratio of cytoplasm to nucleus, and a prominent cytoskeleton resulting in increased background noise (greenish in color). In order to solve these problems I was considering several alternatives, such as changing the fluorescent marker that annexin V is conjugated with to reduce autofluorescent interference, using a different marker of apoptosis (in the place of annexin V), or, if I were to continue using annexin V, I think that incubating with annexin V followed by washing off of excess annexin, followed only then by trypsin treatment could potentially solve one of my various problems (or then again, it might not). Please help me find a suitable protocol for flow cytometric analysis of apoptotic markers in adherent epithelial cells. Additionally, if you know of any studies which utilize such methods, please direct me to them. Thanks in advance.

Consider trypsin is a serine protease and your annexin is a protein.

Here some resources,

Cell harvesting effects on Annexin V staining.
Protocol for apoptotic analysis using Annexin V.
Quite a long discussion about this issue.
Another protocol.

Cheers,
Pedro


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What is the importance of alkaline condition in biuret test?
Biuret test aims to quantify the amount of protein in a given unknown sample. Biuret agent contains copper sulphate, sodium potassium tartrate and Sodium hydroxide. Coppper ions form the complex of purple colour. Sodium hydroxide is added to make the solution alkaline. Why is it needed to make the solution alkaline?

In the Biuret reaction, copper forms a complex with the nitrogen of the peptide bond, that looks like this (Structure 61 from the paper below):

A strong base is necessary to provide the conditions for deprotonating these nitrogen atoms and have the conditions to form the complex. If you want to read this in detail, have a look at this publication:

Coordinating properties of the amide bond. Stability and structure of
metal ion complexes of peptides and related ligands


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What would be the molar concentration of human DNA in a normal human cell?
A diploid human cell has 46 chromosomes. A haploid cell has DNA approximately 3.2 billion bases long. What is the molar concentration of DNA in the cell then? How would we calculate?

Welcome to Biology.SE! Is it a homework question?

What do you mean by "molar concentration of DNA"? Do you "molar concentration of nucleotides" or "molar concentration of DNA strands" or "molar concentration of chromosomes"?

This question seems devoid of practical relevance or any particular biological interest. Why do you ask?

I will assume that be "molar concentration of DNA", you mean "molar concentration of nucleotides".
Cell size
Assuming a cell with a radius of 0.05 nm (nanometer). Assuming a perfect sphere, the volume of such sphere is $5.24\cdot 10^{-4} nm^3 = 5.24\cdot 10^{-11} L$.
Of course, cell volume varies a lot among different cell types. The final result will drastically depend upon the cell volume considered (Thanks to @Roland fo highlighting that in the comment).
Number of nucleotides
In the nucleus
The haploid genome size is about $3.2\cdot 10^9$ nucleotides. The whole genome is therefore $6.4\cdot 10^9$ nucleotides. As there are two DNA strands at each haploid genome, we have to further multiply by two to get $1.28\cdot 10^{10}$ nucleotides. Note that this number could be lower at other moment of the life cycle. What I am computing here is the maximal number of nucleotides per nucleus
In the mitochondria
There are about 1500 mitochondria per cell. Each mitochondria contains about 16,000 nucleotides resulting in a total of $2.4\cdot 10^7$ nucleotidesin mitochondria per cell.
mitochondria + nucleus
$2.4\cdot 10^7 + 1.28\cdot 10^{10} ≈ 1.28\cdot 10^{10}$. That is mtDNA is negligible.
In the mols
The Avogadro number is about $6 \cdot 10 ^{23}$. Hence, there are $\frac{1.28\cdot 10^{10}}{6\cdot 10^{23}} = 3.2\cdot 10^{-14}$ mols of nucleotides per cell.
Molarity
Molarity is defined is defined as the number of mols per liter. It is therefore
$$\frac{3.2\cdot 10^{-14}}{5.24\cdot 10^{-11}} ≈ 0.0006M$$

Nice, but I would add that this depends heavily on the cell volume, which varies a lot between cell types. The cell volume you use (52.4 pL) would be a very large cell: typical mammalian cells range from 1--5 pL in my experience (in cell culture). For such cells, the concentration is an order of magnitude higher, around 5mM. (Of course, the DNA nucleotides are not free, so this "concentration" is artificial.) Also, the "0.05nm" must be a typo, since that would yield a sphere volume of 5.24E-28 L.

But the poster asked specifically about moles of DNA, not moles of nucleotide, mentioning the number of chromosomes. I think the question is pretty silly and best ignored, but if you are going to answer, I think you should do so properly.


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Why doesn't CAS9 cleave the original CRISPR sequence in the bacterial genome?
CAS9 is the RNA-guided endonuclease that cleaves DNA as specified by the RNA sequence and is used to target viruses that infect bacteria. So why doesn't this RNA+endonuclease combo also cleave the original CRISPR spacer sequences (which also have the same DNA?). Is it the same reason that the bacterial genome is methylated (and hence protects from restriction enzymes)? Does methylation also make a difference to CAS9 as it does to restriction enzymes?
This actually was a doubt asked to Eric Lander in this lecture.

It is not the methylation status. The crRNA is not only complementary to the spacer sequence within the CRISPR array but also to the repeat sequence flanking that spacer. The additional base pairing of the sgRNA with the repeat prevents a nucleolytic cleavage by Cas9. In addition, the arrays typically do not contain PAM sequences.
Here you will find a nice illustration:

The explanation regarding complementarity of the 5' handle is true for Type III CRISPR-Cas systems. In type II systems such as Cas9 a protospacer adjacent motif is required for self vs non-self recognition.
PS: If this question was asked to Eric Lander and he was obviously not able to answer (otherwise why is the question asked here?) then I am not surprised as to why his "Heroes of CRISPR" is so inaccurate and misrepresenting.

Please add some references to your answer.


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Do death rate and birth rate become equal at replacement fertility rate?

A population transitions from stage 3 to stage 4 when the fertility rate reaches the population replacement level of 2.1.
My question is that if the population replacement level reached, shouldn't the net growth rate be zero? i.e., birth rate = death rate? But in the figure, in stage 4, birth rate > death rate and there is still a population increase.
How is this so?

The transition to stationary populations is between stage 4 to stage 5 in all exemples of the DT model that I've seen. Not between stage 3 and 4. This is also what is being implied in the figure that you've included. In your link they also write:

Countries like India in the third phase of demographic transition have fertility rates that have declined significantly from previously high levels but have not reached the population-stabilizing "replacement level" of 2.1 children per woman.

This is not saying that countries reach the replacement level 2.1 at the end of stage 3.
The same stages are also described at the Wikipedia page on DT and at populationeducation.org.
So you are correct; at replacement levels, populations shouldn't increase and the net growth should be zero.


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Are any arthropods poisonous to the touch?
I'm particularly interested in whether any insects are poisonous to the touch.  Note that toxic-bristled caterpillars are actually venomous, since in all species I'm familiar with, the bristles puncture the skin.  If there are any arthropods poisonous to the touch, I'm also curious as to what the most dangerous one is, but that may be beyond the bounds of this site.

The blister beetle genus Meloe, also known as oil beetles, secrete an oily substance containing a poison called cantharadin which causes blistering and swelling of the skin.

Source: http://statebystategardening.com/state.php/articles/do_not_touch_these_backyard_bugs

I agree with Kurt, but there is a great deal of variance in the concentration of cantharadin among blister beetle species. Some millipedes (Myriopoda: Diplopoda) also ooze toxic secretions from glands along their sides. http://www.sciencedirect.com/science/article/pii/S0305197815001167


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Evolution at a glacial pace: how does it work?
Some trees are very long-lived, such as the Great Basin Bristlecone Pine and the Giant Sequoia (up to 4,800 years old).
How does natural selection and evolution affect such long-lived organisms?  Their DNA has remained unchanged for thousands of years.  Mutation can't hope to change the DNA of the entire tree.
I don't understand how they can hope to be able to adapt to a changing environment.  And yet the    Sequoioideae subfamily has existed since at least the Jurassic, so they must have a winning strategy for survival.
Please help me understand how a species such as this can adapt.  And what natural pressure would select for such longevity?

For some clarification, evolution isn't observed within individuals; it's observed in populations, and over multiple generations.

@Harris has correctly noted that evolutionary time is better measured in generations, rather than absolute years. You also have mentioned the Jurassic period - that is 200 million years ago - this is still hundreds of thousands of times longer that the lifetime of Sequoia given in your question (could you provdie a reference for this number?)

@Harris I am not quite sure what you mean by 'evolution isn't observed within individuals; it's observed within populations' - could you clarify that?

@user438383 The question seems to frame this as individual trees' DNA changing to adapt, which is not a typical context to consider evolution in.

Consider that a long-lived individual can produce offspring - in this case, seeds - over many years.  In the case of the Giant Sequoia, seed production can begin as early as 10 years, and is heavy from about 150 years, which means about 2000 years or more of producing genetically diverse seeds, of which only a few individuals will survive.  https://www.srs.fs.usda.gov/pubs/misc/ag_654/volume_1/sequoiadendron/giganteum.htm


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Mammalian scales
Many small mammals have scaly skin on their tails and sometimes limbs. The examples can be found among rodents (rats, degu, scaly-tailed squirrels), insectivores (shrews, desmans), oppossums, musky rat kangaroo. There are much more prominent examples like pangolin scales but I would like to concentrate on as simple things as possible.
I would like to know the answers or at least what is known on the following quiestions.

Are scales of these different mammals actually something similar or
is it just an illusion?
Does the scaly pattern at least in some cases represent some primitive characteristic of a common mammalian ancestor?
In case of positive answer on the previous question is there any connection to the scales of the diapsid reptiles? As I understand the latter are built from $\beta$-keratin absent in mammals but perhaps there are still similarities or even a common origin.

For now my search on this topic resulted in some contradictory claims without any solid references. I would update in case I find anything that seems relevant.

https://biology.stackexchange.com/questions/1138/what-did-pangolin-scales-evolve-from ......... http://thomas-hopp.com/blog/2013/01/26/even-more-dinosaur-skin/

@com.prehensible Well, there's a reference on pangoline scale evolution (which I sadly can't read right now) but from reading the abstract I'm not sure that would answer my question. And surely the answers on that question don't answer mine. I probably shouldn't have mention the pangoline at all...

The most primitive mammals from the list are probably Opossums and Beavers, which have the most reptile like tails of all. http://dolly.jorgensenweb.net/nordicnature/wp-content/uploads/2014/04/beaver_tail_Jamtli.jpg ......
http://media.gettyimages.com/photos/closeup-of-beaver-tail-northern-ontario-canada-picture-id128069910

@com.prehensible ...or their ancestors had furry tails and this is actually a derived trait. Contrary to cartoons platypus has furry tail!

@com.prehensible For me (not possessing any considerable knowledge on this topic) this is main weakness of the idea that protomammals had scaly tails and limbs - as far as I know monotremes don't have any scales. Though that may prove nothing as they are not very diverse and experienced considerable evolution themselves

It interesting to note though that some mammaliaformes (not even mammals) like castorocauda seem to have scaly tail though that could be again a convergent evolution.

The fossil of castorocauda from 140million years ago is simply incredible, it is conserved with hairs and scales, totally awesome mammaliaform, they must have been warm blooded and perhaps even bore live young. very amazing. https://news.uchicago.edu/sites/default/files/images/image/20150216/uxomsdakjb1905320150216.jpg

from general reading, I saw today that placentals and marsupials split 160mn years ago, and that the oldest human relative fossil is 2 rat teeth from 145mn years ago. rhino's can be a bit similar to lizards: https://www.google.fr/search?biw=895&bih=530&tbm=isch&sa=1&ei=jQQzWrqgLszyUp6wvXg&q=rhinoceros+skin&oq=rhinoceros+skin&gs_l=psy-ab.3..0l3j0i8i30k1j0i24k1l5.10814.13050.0.13273.12.9.0.3.3.0.81.618.9.9.0....0...1c.1.64.psy-ab..0.12.623...0i67k1j0i5i30k1.0.CjBRmWxVvxE#imgrc=ZqL7FEToFozO0M:


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How do tear glands secrete tears?
Keep in mind I'm not asking what the function of tears are or what causes tearing,(there's a lot of good answers on it already). My question is: how exactly is the tear gland able to actively push out fluids when it receives a stimuli? What exactly is the tear gland doing and how does it produce tears? How does it start and stop?


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Is it possible for parsimony to estimate more state changes than stochastic character mapping
I'm mapping states (geographic regions) onto a phylogeny to estimate the number of transmissions between countries.
I'm using two methods, stochastic character mapping implemented in Phytools and parsimony implemented in Mesquite.
I was expecting parsimony to give lower results than stochastic character mapping, as it doesn't attempt any simulation along branches. This is generally true, and the number of transitions between states is generally lower estimated by parsimony. However, in a couple of cases, the number of transitions estimated by parsimony is higher than by stochastic character mapping.
I'm still developing an intuition in this type of analysis, so could someone tell me if this is feasible, or should I be looking for a technical problem somewhere?

If the number of taxa is large enough, an exhaustive search is not possible, and parsimony methods use heuristics to explore the tree space. It is therefore not guaranteed that the most parsimonious tree will be encountered.
This might explain your observation if your tree has a high number of taxa (> 20).
According to wikipedia:

However, although it is easy to score a phylogenetic tree (by counting the number of character-state changes), there is no algorithm to quickly generate the most-parsimonious tree. Instead, the most-parsimonious tree must be found in "tree space" (i.e., amongst all possible trees). For a small number of taxa (i.e., fewer than nine) it is possible to do an exhaustive search, in which every possible tree is scored, and the best one is selected. For nine to twenty taxa, it will generally be preferable to use branch-and-bound, which is also guaranteed to return the best tree. For greater numbers of taxa, a heuristic search must be performed.

How many taxa do you have?


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At what point does muscle mass overcome muscle strength to affect speed?
I'm trying to think in terms of "how fast" someone can do something, like swing a bat or push a crate. Someone might have a lot of muscle mass, but that also increases how much mass an arm has to move which also increases the torque. Is there anything referable in biology that has found at least some estimate of where these two factors trade off?


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Is there a way to determine how far and how fast an animal can run for based on geometry?
I was looking at research and finding that drastically different animals can fall under the same brackets for how far and how fast they can run, or that similar animals can fall under different brackets. For instance, a kangaroo could hop at 40mph for a couple miles, meanwhile an elephant can also run about 40mph but for only a couple miles. They're very differently shaped animals, and yet have a similar ratio of their sustained run to their stamina.
Conversely, humans can run for a very long time but maybe no more than 20mph for those in great shape, though they can do it for many miles, over 20 miles which is longer than an elephant can run for. Bears have very similar legs and feet to humans as they are both larger plantigrade mammals, but they can run at 35mph for their top speed and otherwise don't have as much stamina as humans.
Felines and canines are often thought to be similar in many ways. Wolves are known for being able to run and walk for long distances, often having more stamina than their prey and moving 10-30 miles in a day. But, their top speed is only somewhere in the range of 20-35mph. Lions have very similarly shaped bodies and yet are more adapted to run short distances at around 50mph. Similarly, dogs can run for long distances, but cats can jump much higher and not just in proportion to their body length but in terms of absolute length, despite having very similarly shaped bodies.
The reasons for these differences must have something to do with the combination of the geometry of their vertebral column, legs and feet over which their muscles are shaped as well as the weight of an animal. If an elephant was lighter, it would surely run much faster, probably comparable to a horse as its feet are already ovaloid and digigrade. And, if a dog was lighter, it would probably be able to jump higher than a cat. If humans were more massive, then they probably wouldn't be able to run as far, but would probably as fast or faster due to increased muscle mass that compensates. A horse and other horse-like animals seem to have a very good ratio of geometric features to mass that lets them run both very far and very fast.
With all this diversity in mind, what common denominators can be found to account for how the geometry of an animal determines its speed for its given mass?
For instance just as a very crude estimate, I would say animals with particularly long legs that are more closely aligned with the angle of their vertebral column have a tendency to run the farthest, but also the slowest. This might have something to do with how the elasticity of longer muscles and tendons is more efficient for repetitive motion, but not necessarily for propelling a body forward by keeping the force transferred from feet perpendicular to the ground up the leg and in the direction of motion.

Somewhat related: Why don't mammals have more than 4 limbs?

Is there anything about the anatomy of a given animal that would suggest it has more slow or fast twitch fibers?

It's not entirely a matter of geometry, but of differences in muscles, lungs, and circulation.  For a good example, read about the extreme endurance of sled dogs.

Couldn't those differences simply be attributed to training? I'm referring more to a purely elementary setting.

No, the differences between sled dogs and other breeds of dog are more basic than training.  They have better endurance &c than similar-sized dogs of other breeds that recieve the same training.


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Is the ACh receptor more permeable to sodium ions?
The AChR is permeable to sodium and potassium ions only and has a reversal potential of 0mV.
However the Nernst potentials for sodium and potassium ions is ~ +60mV and -88mV respectively. Taking a simple average of these two potentials would give an expected AChR reversal potential of -14mV; but that is not what we see.
My question is whether the reversal potential is pulled up to zero because of a greater conductivity to sodium than potassium ions, and if so, how the AChR selectivity filter achieves this.
Thanks!

Short answer
No.
There are differences in Na+ versus K+ permeability, but you have it backward: potassium is actually slightly more permeable; however, these differences are not the only factors influencing the reversal potential, and also, the reversal potential for a nAChR need not be exactly 0 mV.
tl;dr to the long answer
You need to sum before taking ratios rather than take a difference of ratios when computing a reversal potential for multiple ions together.
Before we get into the weeds...
In most sources you will hear something like the reversal potential for a nonspecific ligand-gated channel like nAChR is "about 0 mV" - this is going to vary in different cell types, in different conditions, with different recent activity levels, with different versions of the receptor, etc.
What's important to remember in all this is that -14 mV is also about 0 mV... In the context of excitable cells, what is most important is the reversal potential relative to the threshold for firing a spike or activating other channels. That said, I'm not actually saying the reversal potential for nAChR is actually -14 mV, there are a couple other factors missing...
What you are missing
The big one you are missing is that the concentrations of the ions matter, not just their ratios. For the reversal potential of a single ion, all we really care about is the ratio inside and out, which is found in the Nernst equation.
Averaging the reversal potential for two major ion species, like you have done, gives you a pretty good ballpark estimate (afterall, -14 mV is also about 0 mV!).
To get the actual reversal, however, you'll need the Goldman Equation.
We can simplify the Goldman equation for just Na+ and K+ in fairly standard conditions to something like:
$61.5 \mathrm{mV} * log_{10}(\frac{P_{Na} [Na^+_{out}] + P_{K} [K^+_{out}]]}{P_{Na} [Na^+_{in}] + P_{K} [K^+_{in}]]}$)
If the permeabilities are both :=1, and the concentrations of Na and K are equal and opposite, then indeed you will get zero. However, if that was true, you would also have equal and opposite reversal potentials for Na and K alone in the cell: in the numbers you gave, that isn't the case.
I'm not sure what numbers you used exactly, but I'll use my own example. If potassium is 5mM out, 140 mM in, the reversal potential will be -85.6 mV for potassium. If sodium is 140 mM out, 12 mM in, the reversal potential will be 63.1 mV for sodium (you can check my math with the Nernst equation).
If you combine these numbers in the Goldman equation above, you will get -1.2 mV: closer to zero than your -14 mV estimate.
They are so close because the ratio (140+5)/(12+140) is a lot smaller than the difference of the ratios (5/140) and (140/12): order of operations matters.
This is assuming identical permeabilities

However, the permeabilities aren't actually identical
There are many papers measuring relative permeabilities in nAChRs, I just chose one randomly as an example (happened to be the first Google Scholar result).
Nutter and Adams 1995 found the relative permeability of several monovalent and divalent cations, with Na as a reference:

Therefore, potassium is actually slightly more permeable than sodium. However, there are also other important ions that could contribute, even if they are found at lower concentrations than either sodium or potassium, and the example ion concentrations you find in a textbook might not apply in the systems you are studying. A source that says nAChRs are only permeable to sodium and potassium really just means that they are not permeable to another other important high-concentration ion: chloride. They are also simplifying things a bit for you, which is okay.
If I use the Goldman equation quickly with these data, I get a reversal potential (with just Na and K, ignoring other ion species) of -5.9 mV: still "about 0 mV" and still closer than your original -14 mV estimate.
But how are different ions with the same charge showing different permeabilities?
This is better off as a separate question, and probably easier to address with a more extreme case, like in selective sodium or potassium channels. However, like in those channels, in channels that we call "non-specific", the particular arrangement of amino acid residues (especially charged ones) at the pore can favor particular ions because those ions differ slightly in size.

Nutter, T. J., & Adams, D. J. (1995). Monovalent and divalent cation permeability and block of neuronal nicotinic receptor channels in rat parasympathetic ganglia. The Journal of general physiology, 105(6), 701-723.

I'm really happy with this answer! I hadn't really appreciated the importance of the magnitude of ion concentration as opposed to just their ratios in setting membrane potential.  Thanks for taking the effort to correct my misconception:)

@ogu01 I really like the simplicity of the Goldman equation: sort of the "F=ma" of neuroscience and other disciplines where excitable membranes are important; I think it's really helpful as a student of these sorts of topics to just sort of "play" with it and make up your own scenarios and test them out. This will help the concepts make better sense. Best of luck to you!


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How to attain a deep conceptual grasp of key atomic/molecular/genetic/ notions?
It's a total noob question, I know.
I'm a layperson trying to come to grips with basic scientific terminology. I always face a conceptual hurdle in trying to understand micro-talk. The way I'm using the expression 'micro-talk', I take it to refer to any kind of discourse that relies extensively on concepts that refer to unobservables like DNA, adenosine triphosphate, other molecules/compounds, chemical elements, atoms, etc. i.e. the kind of quasi-tangible entities that we can never perceive directly owing to our particular evolutionary history that prioritized engagement with mesoscopic objects.
Whenever I read anything in an introductory textbook, the talk of such entities is always presented as a given to me. It's not explained on how on earth we know about them (or even if such explanation is given, it's usually quite shallow and circular i.e. it makes references to the entities in question). I can recite, or rather parrot facts about them just fine. If you ask me why a second magnesium ion is important for ATP, I retort that that's because of its functional role in regulating kinase activity. I might be able to successfully make certain inferences between sentences that involve such concepts. So I might even successfully pass a scientist's Turing test, but that's all there is to it. I don't really have an understanding of what I'm talking about. I feel like I'm a robot or a medieval scribe.
How can I get over this conceptual chasm? Learning about a historical development of a particular discipline might help, but I need to find a way to systematize my study and I can't have a recourse to university right now (even if I did, I'll face the same conceptual hurdle). I have library loans and will to study, but I haven't internalized a good number of micro-talk related concepts and they feel so foreign to me.
This is quite maundering, but I couldn't put it any more succinctly. If there's anyone who experienced a similar frustrating feeling to the one I've described, I'd be very grateful if they could offer me some tips. Thanks a lot.

You should study chemistry, and the history of chemistry would also be good, like atomic models, Rutheford, Bohr, etc. Some software of visualization of molecules, like RasMol, could help as well.

here are chemistry animations, if you learn well with visuals. https://www.youtube.com/results?search_query=chemistry+animations&sp=EgIQAw%253D%253D

Although I think this question is off-topic here (is there an eduction of psychology SE?) I find your attitude interesting. It may reflect a general attitude of people who are put off by molecular sciences or your own particular research mind. The question is whether it would help you reading  texts that described the way the atomic theory and then molecular theory was developed and the evidence supporting them. Or would the uncertainty be still too great for you. How mistakes (e.g. phlogiston) persisted for years before being discarded. How simple theories had to be revised. You could try.

@David, I think that would definitely help. I couldn't find any historically oriented textbooks for either chemistry or biology. The closest example I can give comes from math - Kline's 'Mathematics for Nonmathematicians' (but being well versed in the topics covered in the book due to math background, my evaluation might be very skewed). I did come across history books on chemistry, however they were clearly aimed at experts and presupposed substantial knowledge on the reader's part

When I was at secondary school in the 50s (sic) the text books (physics, especially) adopted that approach, partly for contemporary pedagogic reasons, partly because less was known then. I'm not sure how you would get hold of a (more condensed) chemistry text with a similar approach today. Many/most major conceptual breakthroughs did not follow the "scientific method", but involved ideas of how matter might be, for which support was slowly obtained by the results of experiments, generally inconclusive in themselves. The logic of the ideas appealed to me, so I could accept the uncertainty.

Just to clarify, I'm not craving Cartesian certainty, divested of all doubts. I articulated it clumsily in the OP, all I want is for these concepts to 'click'. I can follow some inferential connections between them, trace the logic of their behaviour even. Yet I feel like I'm learning how to move chess pieces without grasping why the rules are set up the way they are (in the case of chess, it's a matter of convention, which is where the analogy breaks down). The concepts are free-floating and only connected to colourful idealized pictures in textbooks.

For me a lot of clicking happened thanks to structural biology. Actually seeing how each molecule of that enzyme looks physically, and how it interlinks with others, made everything much easier to imagine. Try adding "PDB" (or PDBe if you prefer the UX) to a search for a protein and usually you'll find something nice to look at. Also, this: https://www.youtube.com/watch?v=X_tYrnv_o6A

I'm assuming you have a reasonable high school education otherwise you probably wouldn't have posted your question.
Do a basic science course and/or read - maths, physics, chemistry, biology texts. 1st year university level should be good.
If there is anything you don't understand in these texts, go to more basic books - plus Wikipedia is good for the sciences (I wouldn´t like to read them on, say, the Arab-Israeli question), but I've never seen any egregious errors in the scientific area!
Then read Klug and Cummins "Concepts of Genetics" from cover to cover.
If there is anything you don't understand in Klug and Cummins, go back to basic texts.
I had a good background in the  sciences and then majored in Genetics with minors in Biochem, Microbiology and Immunology. I read that book from cover to cover taking notes in 3rd year (of a 4 year degree programme) and have done very well in the field.
The book covers the history of the discoveries in a very readable and approachable fashion. Obviously it is no substitute for doing a degree in the subject, but if you really wish to at least have a good understanding of the science, you could do worse than read that text!
You could also read popular science books aimed at the "interested and educated layperson" - Stephen Jay Gould, Richard Dawkins for example. Try National Geographic and even Scientific American or New Scientist. You, at least intially, will have to make a real effort, but it is very rewarding - there is nothing more fascinating than biology generally and molecular biology/genetics in particular! Best of luck on your journey!


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What's the relation between Kinase, Phosphatase and ATPase, GTPase (GTP/ATP)?
I'm wondering what's the relationship between Kinase, Phosphatase, ATPase (ATP) and GTPase (GTP).
For example, when reading online the impression is created that ATPase is a type of Kinase (?). But I can't find any explicit information about it.

Related, with good answers: https://biology.stackexchange.com/questions/23589/what-is-the-difference-between-a-phosphotransferase-a-phosphatase-a-phosphoryl

Please do some homework before asking basic questions of this sort.

Enzyme names usually refer to the substrate of the enzyme, i.e. the molecule or chemical group that the enzyme targets and then removes or modifies.
Kinases are enzymes that add phosphate groups, usually to other proteins. One of the older enzyme classes that have a more "creative" name. Phosphatases remove phosphate groups.
In signalling pathways, kinases often transduce signals and phosphatases shut them down when their job is finished.
ATPases and GTPases target ATP and GTP respectively and catalyse the removal of one phosphate group by hydrolysis, the product being ADP or GDP. This makes them a type of phosphatase.
Many proteins are ATP/GTPases but have different names because there's a more significant function to name them after. Usually the ATP/GTPase function serves to deliver energy for the main function. Your impression might be caused by an enzyme which is both a kinase and an ATPase because it transfers phosphate groups from ATP to a target protein.
Enzymes that target ADP/GDP and add another phosphate group are called ATP/GTP synthases (rather than kinases).


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Why aren't white blood cells called pus cells?
So, pus is just a concentration of dead white blood cells that results from your body detecting an infection or a foreign body that needs to be removed and sending a whole bunch of white blood cells to fight it, right?
Why aren't they called pus cells, then, if pus is the form they take when they're concentrated enough to be visible to the naked eye?

Blood clots, among other things. Why don't we just call red blood cells "clot cells"? Because that's not all they do. Just like WBCs.

Because they're the cells that make up your blood, and they're why it's red when you cut yourself and you can see it flowing? Same reason why muscle cells are called muscle cells and nerve cells are called muscle cells. But you can't see the white blood cells, so why aren't they named after the tissue that they form?
Also, aren't the platelets the ones that cause the clots, anyway?

They are called white blood cells, because they look white when purified. So in fact, their naming is following your expectations. https://en.wikipedia.org/wiki/White_blood_cell#Etymology

Pus is comprised of two types of cells - neutrophils and macrophages.
These are cells sent by the body to combat pathogens.
There are a variety of other leukocytes(WBCs)(like lymphocytes, which is another broad term among many others) in the body that aren't part of pus which is why they aren't called pus cells.


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How do farmers tell if their fruits are sweet without eating them?
A relative of mine tells me that when she goes to buy fruits, she asks the vendor if the fruits are sweet. Surprisingly, the vendor is able to tell (the vendor is apparently willing to divulge this information because my relative is a long-time customer of the vendor). In turn the vendor gets the information from the farmer.
How can the farmer tell if their fruits are sweet without eating them? The only thing I can think of is they eat a very small batch, e.g. if they produce 100 apples then they eat one and use that to infer if the remaining 99 apples are sweet - but can we say with certainty that if one apple on a tree is sweet, then all the other apples on the tree (or on the farm, even) must also be sweet? If we can, what is the biological basis for this inference?
If this is not the method farmers use, how else can the farmer tell if their fruits are sweet without eating them?

What exactly do you mean by "sweet"?  Are you using it as a synonym for ripe?  There are many ways to tell if fruit is ripe - color, whether it's hard or soft to the touch, how it smells, and so on, and these vary by the type of fruit.  It's simply a matter of practice.  If you mean sweet, that will also depend on the type of fruit: a good number aren't - quince, for instance, or cornelian cherries. (Making a batch of jam at the moment, and you have to add quite a bit of sugar to make it palatable.)

@jamesqf "sweet" is not ripe; it means one of the five basic taste sensations. If you are concerned about how some types of fruits might not be sweet, then narrow the question and consider only apples.

In the case of apples, you know the sweetness (and other characteristics) primarily by variety - cooking apples will be less sweet than eating apples, and crabapples are distinctly tart.  Another factor is ripeness, which for apples you usually judge by the skin color, and somewhat by the season.  As a grower, you have learned that for instance your Red Delicious apples are ripe in October.

A relative of mine tells me that when she goes to buy fruits, she asks the vendor if the fruits are sweet. Surprisingly, the vendor is able to tell (the vendor is apparently willing to divulge this information because my relative is a long-time customer of the vendor). In turn the vendor gets the information from the farmer.

Whether a fruit is sweet is not a classified information: a good groceries store would typically offer several types of the same species of fruit, depending on their sweetness, crunchiness, how long they can be conserved, etc. This is in order to suit the tastes of the customers (not everyone likes extremely sweet apples that desintegrate in your mouth), their purposes (eating raw, making jam, cooking purée for a baby), etc.
How do they know? The varieties of fruits with different tastes are a result of breeding, just like different varieties of cows, dogs, etc. It is not uncommon to see charts like this one.

Does this mean that all apples of a specific kind (like "Ginger Gold") will taste the same? If so that's certainly something I never noticed, will pay more attention next time.

@Allure they will not all taste exactly the same, and on occasion one may encounter a bad batch. However, in comparison with other varieties, the taste remains more or less uniform.


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Is a part of the spinal cord from the mesoderm?
The caudalmost part of the neural tube is formed by the caudal eminence. Isn't this mesodermal? So does it mean that, a part of the spinal cord is mesodermal in origin?
Does it have any significance apart from being something just academic?

@JM97 zara ye bhi pls :)

The caudalmost part of the neural tube is formed by the caudal eminence. Isn't this mesodermal?

No,the neural tube is not mesodermal at caudal end.
According to Gray's Anatomy:

At the time of caudal neuropore closure, the caudal midline cells are generically termed the caudal eminence (O’Rahilly and Müller 2004). A specific population of mesenchymal cells, the caudoneural hinge or junction, shares the same molecular markers as the primitive node. These cells aggregate at the midline and undergo mesenchymal/ epithelial transformation, producing a cellular cylinder that is contiguous with the caudal end of the neural tube. Further elongation of the caudal neural tube involves cavitation of the neural cylinder.

So, the cells in the caudal eminence form a solid cylinder(medullary cord) which is made hollow by elongation of neural tube. Therefore, mesodermal cells of caudal eminence are not forming the caudal end of neural tube.
Let's see the process of neural tube elongation from the citation given in the Gray's textbook:

Abbreviation used can be seen here
Schematic diagram can be seen here


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Is the knee locking mechanism present in animals?
We study in human anatomy that when the knee is in full extension, the femur slightly medially rotates on the tibia to lock the knee joint in place. This reduces the work required to be done by the hefty thigh muscles. This happens in the knees in humans since they are the weight bearing joints.
So, is the mechanism of locking present in other animals? If yes, is it even in the fore limbs or just the hind limbs?

Could you please paste in a link here? of an appropriate result? @Fang

https://en.wikipedia.org/wiki/Stifle_joint Equids use this stifle joint to stay standing while they sleep.

@fang thanks a lot! It happens to be similar to humans, the mechanism. But locking happens only in the knees in bipeds. This makes sense since our liwer limbs are the ones that are wt bearing. is there a similar mechanism in quadrupeds in their fore limbs as they too are weight bearing.

Yes, the mechanism of patellar locking does occur in quadrupeds too. Although they are 4 limbed, a major portion of the weight is borne by the hind limbs. This is known as the stay apparatus and includes the mechanisms of Patellar locking, reciprocal mechanism and check apparatus.
On the other hand in the forelimb, although there is no locking mechanism as such, there exists a neat difference from the human anatomy. Human forelimbs are majorly adapted for manipulation but for quadrupeds, they are weight bearing. There exists what is called the stay apparatus - which includes the suspensory apparatus and the check apparatus.
For a detailed explanation for the interested reader, heres a helpful link - https://en.wikivet.net/Stay_Apparatus_-_Horse_Anatomy


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Where does craniocaudal closure of anterior neuropore start?

Closure of the cranial neuropore is bidirectional, and final closure occurs in the area of the future forebrain. Closure of the caudal neuropore is strictly craniocaudal and finishes at the level of the second sacral segment.

This is what Larsen's Embryology says. I understand that neurulation starts somewhere in the area of the first five somites and then proceeds in both directions - cranial and caudal. The caudal neuropore is closed on day 26 by neurulation in this direction.
But, the cranial neuropore is closed not only by this cranial wave of neurulation but also by another one incoming craniocaudally and the point where they both meet is of final closure. (hence bidirectional)
My doubts - pls correct if any of my interpretations are wrong. Where is this second craniocaudal wave originating? Where is the final point of meeting (I suspect linea terminalis or anterior commissure) ? Could anyone post a picture or a reference to understand this visually (both waves of neurulation)?
PS. I am not talking of primary and secondary neurulation. Which is different and concerns the caudal eminence.

Where is this second craniocaudal wave originating?

It begins in the prosencephalic region adjacent to the chiasmatic plate.

Where is the final point of meeting (I suspect linea terminalis or anterior commissure) ?

Cranial linea terminalis represents the zone of closure of cranial neuropore.

Could anyone post a picture or a reference to understand this visually (both waves of neurulation)?

Sources:
1: https://www.ncbi.nlm.nih.gov/pubmed/11948562
2: https://goo.gl/RLmQcj

Thanks!  A picture is truly worth more than a thousand words! I was breaking my head for so long, only if this pic was put into the books!

Links for them can be found in gray's anatomy.


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Is there any relationship between the height of a tree and the number of branches emerging from the main stem?
Is there any relationship between the height of a tree and the number of branches emerging from the main stem?
I am particular interested in spruce or fir.

The height is only one of a few factors; also the species and environment are more significant. A spruce growing in unshaded location may have branches to ground level while the same species in a dense woods will only have branches at the top. A southern pine ( in the US) is often 100 ft tall with all the branches in the top 30 ft ; these trees drop the lower branches because of limited light and because various vines climb into the lower branches ( until the branches die and fall).

My own observation is that most conifers (at least those growing in the western US), and at least some deciduous trees, seem to form a new set of branches each year as the tip grows.  (And likewise with sub-branches.)  How far that growing tip extends during the year depends on species, weather, &c.  So if you counted branch sets (and the knots where low branches had died back), you might have a good estimate of the tree's age.

Not exactly about height-to-branch ratio but an answer more about branching geometry in general.
This is my interpretation of a related question on Reddit, "What determines when/where a branch will grow on a tree?" especially from one answer which I've quoted below. It clarifies a primary mechanism involved. The apical meristem (leader branch / tip of the trunk) releases a hormone, auxin, and as it grows generally upward the concentration of auxin decreases. Too close to the apical meristem and too high auxin, no grow; just the right concentration will generate new branches.
As for the arrangement of hotspots which generate new growth, here's an interesting video on the geometry of plant growth. Not so much about height-to-branch relationship, but it does share important concepts about branch geometry. Basically, branches are forming so as to maximize distance from nearby, previously established branches. All of this seems to be a way to optimize space.
In reality, there are other factors like competition and damage which factor into tree growth. A pristine spruce or fir will have a distinct Phi-like arrangement of branch nodes, as the video linked above describes. How well each branch grows, if at all, will be more complicated.

Basically what you're talking about is phyllotaxy, or the patterning of lateral organs (leaves, branches, etc.) around the axis of growth.
  Some plants will arrange organs in a spiral around the stem as it
  grows, or others will alternate from side to side. This varies a lot,
  but always follows a fairly simple geometric pattern. This will
  produce buds in specific areas, and is the basis for the patterning of
  branches that you see in mature trees. The actual biophysical process
  that arranges this patterning relies on the concept of a morphogen.
  These are chemicals that can exist in greater or lesser concentrations
  across a plant tissue. Specifically, we're talking about the
  distribution of auxin across the surface of the shoot apical meristem.
  The details are quite complex (and the details super controversial!)
  but suffice it to say that the plant cells transport auxin to
  neighboring cells based on feedback loops that produce spots of high
  auxin concentration. The spots with high auxin develop into lateral
  organs (leaves). You can model with computers and recapitulate
  observed phyllotaxy seen in nature.
Now, I'm sure you've noticed that trees don't have well-patterned
  branches. Still, this very well organized structure is the basis for
  plant architecture. Look at young tissue or flowers, and you'll easily
  see these patterns. But back to branches.
When a lateral organ is formed, it is accompanied with an axillary
  meristem and a segment of stem. This basic structural unit of plants
  is called a phytomer. Now, the axillary meristem can do a few things.
  For trees, it can produce leaves, a flower, and/or make a branch. The
  'algorithm' that determines what happens will vary from species to
  species and depend on things like apical dominance and environmental
  factors (e.g exposure to light in that area). Some of these axillary
  meristems will become branch meristems, and this is somewhat random
  from a patterning perspective. This is why most trees don't follow
  strict patterns. Over time, some branches will grow at different
  rates, others will terminate, and successive branching decisions will
  determine it's overall form.
Most trees can also form meristems de novo from tissues. If you've
  ever seen a forest tree suddenly exposed to light (from a neighbor
  falling down) you'll know what I'm talking about, as the trunk might
  be covered in leaves. I haven't ever studied this, but I presume that
  this process is quite random, but I also don't think that it's a major
  influence on tree architecture.

via Reddit user Sluisifer


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How to quantify and measure phenotypic variation?
It is easy to quantify and measure genotypic variation, because genes are digital, like the 1's and 0's of a computer. You just check how many places the gene "letters" A,C,G,and,T differ. But how does one quantify and measure phenotypic variation? The reason I am asking this question is because there are several species, like dogs and also us humans, where their genotypic variation is very small, but, at least intuitively, the phenotypic variation is large compared to their genotypic variation. Humans of different races look very different from one another, and different breeds of dogs look even more different, despite, in both cases, being extremely genetically similar. Has any book or paper or text proposed a rigorous definition to quantify and measure phenotypic variation?

It depends on the phenotype you're quantifying. If you want to quantify height, for example, just measure it and record the number. However, you seem to be implying "overall" phenotypic variation of all phenotypes. You may be interested in looking up "PheWASs," or phenome-wide association studies. You may also be interested in the correlation of every phenotype to every other phenotype and every phenotype's variance.
Also, phenotype extends beyond how something "looks" to disease susceptibility, protein expression, behavior, and internal organ structure. You'd have to take all of this into account, which would be difficult. Perhaps something analogous would be studies of protein expression: search for "transcriptome -wide association study."
Lastly, you have a misconception about the genotypic variance of humans and dogs. It's correct that small genotypic variation can lead to large phenotypic variation. However, humans have a large degree of genetic diversity between us, and dogs also have a decent amount. You are not alone in asking this question. One authors said "The domestic dog displays greater levels of morphological and behavioral diversity than have been recorded for any land mammal" (See also: "Behavioral Phenotyping" section of that link, and a related paper). Here are FST charts from Google showing the impressive genetic diversity of our and their species:

(Of course, FST is a poor measure and much of the variation exists outside the way it is shown/defined in these graphs.)


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What is the correct classification of population groups of homo sapiens?
The classification system of the United States census into various races of humans is a bad way to classify population groups of humans, because both East Asians and South Asians are classified the same, yet they look different and are genetically distinct. So, has anyone proposed a more scientifically accurate classification of population groups of homo sapiens?

Basically all the genetic variation of humans is inside the native african populations.  A norwegian and a australian native are more closely related  to each other than two random native Africans are. So the only accurate way to do it would not only group those two asians together but also group them with europeans and native americans. If you split people up enough to get two groups of "asians" then you end up with more than a hundred races the vast majority of whom would be split among the native african populations.
Humans have very low genetic diversity in the first place, and most of our diversity is within our populations not between them, so splitting us up does not make a lot of sense. We end up doing it mostly on superficial variations.
Source


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Reference request for the evolution of faces
We humans have faces, as well as many other animals, like cats, dogs, monkeys, etc. But there was a time on planet Earth before there were any faces in living things. I am currently very interested in how faces evolved. Is there any book or paper on this topic? I would like some references.

What is and isn't a face? Do mice not have faces? What about a crocodile? A fish? A fruit fly? If any of those do not have a face, what makes what they do have not a face?

To expand on Bryan's question: how is it different from the evolution of heads?

@MaximilianPress A head of lettuce, for example.

If what you are interested in is really the evolution of heads (which I think imply faces), then cephalization is what you are looking for.
Namely, when bilaterally symmetric organisms colocalize sensory organs, feeding apparatus, nervous system, and in most cases a brain.

Fig 1: Wikipedia's figure showing where cephalization occurred.
Note that starfish and other echinoderms lost their ancestral cephalized state and went back to radially symmetric headless animals!

Interesting article in Nature: https://www.nature.com/articles/s41586-023-06669-2 "This finding suggests that from the perspective of ectoderm patterning, echinoderms are mostly head-like animals and provides a developmental rationale for the re-evaluation of the events that led to the evolution of the derived adult body plan of echinoderms." - perhaps they're more bodyless than headless!

@BryanKrause woah. biology is weird!

@MaximilianPress Perhaps you are the one who is weird, he who has a strange body hanging off its head.