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How does allele dominance work in polyploid organisms?
You know how there are tables to demonstrate allele dominance in diploids, such as the table found in this question?
Well, I was wondering how this works with tetraploids, hexaploids, octoploids, etc.
One might assume that you would need a four-dimensional table for tetraploids, a six-dimensional table for hexaploids, and an eight-dimensional table for octoploids.
One might assume that if you have an octoploid with a gene that has one dominant allele and seven recessive ones that the dominant trait would be expressed.
One might conclude that recessive traits would be expressed a lot less often in octoploids than in diploids in a population that commonly has both kinds of alleles.
Are all three of these assumptions correct? If not, what is the truth?

Dominance works in the same way.
However, polyploids have complex inheritance patterns!
1. Punnett square for polyploid inheritance

One might assume that you would need a four-dimensional table for tetraploids, a six-dimensional table for hexaploids, and an eight-dimensional table for octoploids.

The table you mentioned in this case should be the Punnett square. And its two dimensions correspond to two types of gametes that fuses in sexual reproduction. So even if you want to utilize Punnett square to work with tetraploids, hexaploids, or even octoploids, you still use a two-dimensional table because there are only two types of gametes involved. The fundamental difference is that you have to assign combinations of alleles to the first row and first column of the table instead of a single allele as you would do with a monohybrid cross.
However, deciding what combinations are allowed will be really intricate in this case, depending on two different factors: pairing behavior during meiosis and the resulting chromosome segregation. Variations in those aspects make general rules for polyploid inheritance impossible. In extreme cases, we can consider the organism to be either fully autopolyploid or allopolyploid.
An autopolyploid has more than two complete copies of the genome of a single ancestral species, and in the extreme case we consider the chromosomes have multivalent formation during meiosis and undergo unbiased segregation.
An allopolyploid has more than two complete copies of the genome derived more or less complete from different species, and in the extreme case we consider the allopolyploid has strictly bivalent formation between the chromosomes of a common origin.
This is a monohybrid cross, and it seems familiar and boring, right?

The following pictures depict how to use Punnett square with a tetraploid with two different alleles at a certain locus, and they are really captivating...

In this final picture you may find that the cross has "degenerated" into a monohybrid cross. If we try to depict something more complex, like a tetraploid with four different alleles at a single locus, we will obtain resultsvery different from normal crosses for diploids.

2. Dominance in polyploids

One might assume that if you have an octoploid with a gene that has one dominant allele and seven recessive ones that the dominant trait would be expressed.

This is true based on the definition of dominance:

Dominance in genetics is a relationship between alleles of one gene, in which the effect on phenotype of one allele masks the contribution of a second allele at the same locus.

3. Recessive traits in polyploids

One might conclude that recessive traits would be expressed a lot less often in octoploids than in diploids in a population that commonly has both kinds of alleles.

For this one, you cannot simply assume it because as I've said above, the inheritance patterns for polyploids, including octoploids, can be really complex and dependent on the particular species and the multivalent formation at the particular gene locus you wish to investigate. Thus, it's difficult to predict the the portion of individuals with a recessive phenotype in a population. There are so many intermediate patterns between two extremities of autopolyploidy and allopolyploidy that geneticists have to rely on sophisticated computational models to help them explain the data collected from experiments!
Source:

Rieger, R.; Michaelis, A.; Green, M.M. (1968). A glossary of genetics and cytogenetics: Classical and molecular. New York: Springer-Verlag.
Soltis, Pamela & Soltis, Douglas. (2012). Polyploidy and Genome Evolution. 10.1007/978-3-642-31442-1.


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Backcrossing in Hybrid
Can anyone help me in understanding how backcrossing helps hybrid to achieve pureline?
I have been looking into the references i possess but couldn't seem to find anything

Back crossing is the process by which a hybrid organism is crossed back (backcrossed) into a pure organism. Let's see an example

Organism 1 is heterozygous for a single gene (e.g. a hybrid), which has alleles that we can call $A$ and $a$. We can write that organism's genotype.
Organism 1 Genotype: $Aa$  (100% chance)
Right now, there is a 0% chance that organism 1's genotype is $AA$.
Goal: increase probability that organism 1's genotype is $AA$

One way to achieve this goal is to cross Organism 1 with another organism, let's call it Organsm 2, that is has a homozygous (e.g pure) genotype of $AA$.
So if Organism 1 is crossed with Organism 2 and produces a new Organism 3 what is its genotype? Well, we're not sure.
Organism 3 Genotype: $AA$  (50% chance)
Organism 3 Genotype: $Aa$  (50% chance)
Now we do the same thing again, to get Organism 4
Organism 4 Genotype: $AA$ (75% chance)
Organism 4 Genotype: $Aa$ (25% chance).
This effect keeps compounding, until there is a very high chance that the final organism has a pure (e.g. $AA$) genotype.

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What defines a microbial species?
I know that microbes are not capable of sexual reproduction, thus sorting them into species according to "groups that can interbreed and generate fertile offspring" should not apply.

I was reading on the topic of OTU's (Operational taxonomic units) and they might sound like a good definition for you. https://en.wikipedia.org/wiki/Operational_taxonomic_unit

Here is more info for bacteria, protozoa, and fungi.

Microbe is not a taxonomic unit: there are no microbial species. --- "Microbe" is "an extremely minute living being"---one needs a microscope to see it. And what is the opposite of microbe? Macrobe, of course. Microbe (viz. microbiology, microbiome, etc.) is a very popular, but not very useful, concept.

Your question is relative to the species concept that you are using. Mayr's biological species concept (BSC) is based on the ability to interbreed; a process-based definition. Most biologists use it, but most taxonomists, who are the people who actually describe species, use some variation of the phylogenetic species concept. The phylogenetic species concept is not based on process, but on fixed differences. Fixed differences are evidence of a lack of interbreeding, but the concept is not explicitly based on reproduction. Fixed morphological differences have been used to classify microbes, most often in culture. But currently, microbes are most often classified with a combination of morphological and genetic characters. The small subunit rRNA is sequenced and put through an algorithm for estimating species based on genetic distances. In short, your question depends a lot on which species concept you are using, and whether you would accept a distance-based DNA definition. But species need not be defined reproductively.

This question actually does not have an easy answer. As indicated in a previous answer, the 16S rRNA gene is used by many scientists. Since this is a fairly conserved genetic region, mutations in this region can differentiate species phylogenetically, but it is not a foolproof method. For example, several species of Shigella can yield nearly identical 16S sequences to those of Escherichia coli and debates rage as to whether they in fact should be classified as the same species. Some scientists even deny that there are such things as microbial species, or if there are, that being able to group microbes into taxonomical units is not worthwhile or informative (although these scientists are still in the minority). If you would like to know more about that viewpoint, you can check out the work of W.F. Doolittle. This one is a fun read:
Doolittle, W., & Zhaxybayeva, O. (2009). On the origin of prokaryotic species. Genome Research, 19(5), 744-756. http://dx.doi.org/10.1101/gr.086645.108

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What is this grainy surface on my two-week-old sourdough starter?
I'm baking bread at home as a hobby, using sourdough. After skipping one baking day, I haven't used my sourdough starter for two weeks. When opening the jar in which I keep it, I saw the surface had taken on this unusual look. When viewed from the side through the glass, the contents looked normal below the surface.
The sourdough starter consists of whole rye flour at 100% hydration (flour:water = 1:1). I had removed it from the ripe sourdough on the last baking day and have since kept it in the refrigerator with a lid (only loosely screwed on) for 13 days.
Normally I'm using it already after keeping it for 7 days, and I'm used to the surface turning light gray and dry (but smooth and soft) after that time, which didn't ever seem to be a problem. Now the color of the surface was identical, but it has become grainy, like tiny worms.
I have removed and discarded the top layer (3 mm). It was soft (unlike dried out, crusty, dough) and smelled a bit like fresh yeast. Below that, the contents smelled normal, like very ripe sourdough.
The jar is about 6 cm in diameter and was filled to about 2 cm (→ volume of the starter ≈ 60 ml).

What are we looking at here? Could it be actual yeast cells (or other microorganisms normally found in sourdough)?
Is it harmful?

After 13 days (click for full-resolution version)
Reference pictures
After only 2 days, the starter looks like this:

(click for full-resolution versions)

You're not seeing cells, as you would need a microscope to see them.

I'm not talking about whether we are seeing individual cells. It is clear to me that a single cell is too small to see with the naked eye. But if there are many cells forming colonies, we can see them. My question is if a colony of yeast or other organisms found in sourdough would look like in my picture.

Somebody else has had this problem. I don't think it's a separate species identification problem. There is some abnormal yeast/bacterial growth.

Thanks for the link! I hadn't seen that before, it looks very similar.

No probs. I think it's probably a mold fungi growing over the yeast, or sometimes when yeast is deprived of nitrogen (so if there was reduced air flow) excessive cell division occurs. In any case, in terms of cooking advice I think you probably need to make another starter!

Here's a study about this.

Naturally, when you create dough you expect it to rise in size the following few days. That's just a chemical reaction that allows air to enter the dough body and traps it in tiny bubbles. My theory is that if the dough is not as high as expected that the air has escaped it because of the extra time you left it.
The pattern is not unusual and is the result of the deflation I'm talking about.
It's probably still safe to eat, but the bread won't be as good(eat at your own risk)

The sourdough starter doesn't rise much (because it is taken from already ripened sourdough) and collapses relatively soon after 2 or 3 days. But then the surface is still glossy and darker as in the picture I've included. The starter collapsing is not the issue here.


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Can you tell if a corpse was male or female by only examining its skull?
There are articles that says women have more rounded corner faces than men, than women noses are usually shorter, etc.
But are those (and other features) tendencies or deterministic features that makes you really able to tell if a corpse was male or female, by only examining its skull?

According to textbook of forensic medicine and toxicology by Ks Narayan reddy:
Qualitative differences are:

Male mandible has everted ramus, but female have inverted ramus.
Males have chin U shaped, but it's rounded in females

Quantitative differences:

Suparaorbital ridges are prominent in males but often absent in females.
Mastoid process is wider, longer and blunt in males but is narrow and pointed in females.

And there are many more differences, see the pics below:

Gautam Biswas says you can be 92% sure only via skull.

Please give a reference for this table ("Gautam Biswas" is not sufficient)

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How does heredity work with Endogenous retrovirus?
Q1: If someone in a species gets infected with an endogenous retrovirus, does that mean that absolutely all of their children will have that endogenous retrovirus? Or is it based on chance?
Q2: is there such a thing as an allele for the virus being there, and for it not being there? How does it work?
Q3: how can an endogenous retrovirus disappear from a species? And when it cannot disappear?

For a provirus to be heritable, the infection must occur in the germ line. The initial integration would occur at one site in the genome and thus the locus could be described as hemizygous. Inheritance would indeed be probabilistic, depending on whether an offspring inherits the provirus-containing chromosome or its uninfected homolog.
Eventually, the endogenous retrovirus (ERV) can become fixed or lost in a population by genetic drift and natural selection. Additionally, retrotransposition and, more importantly, reinfection can greatly increase copy number and allow ERV persistence despite a lack of fixation at specific loci. It should also be noted that more recently acquired ERVs exist that have not reached fixation in humans.

References and Further Reading:
Boeke JD, Stoye JP. Retrotransposons, Endogenous Retroviruses, and the Evolution of Retroelements. In: Coffin JM, Hughes SH, Varmus HE, editors. Retroviruses. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 1997.
Belshaw R, Pereira V, Katzourakis A, Talbot G, Pačes J, Burt A, Tristem M. 2004. Long-term reinfection of the human genome by endogenous retroviruses. Proc Nat Acad Sci 101(14):4894–4899.


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Pedigree Probability, Autosomal Recessive Trait
So, I thought I understood how to calculate the probability for a pedigree, until I came across this answer in my textbook. The question is: what is the probability the offspring of IV1 x IV2 will show the recessive trait? Assume individuals outside the family are not carriers of r unless there is evidence.
White = Dominant phenotype, Black = recessive phenotype.
What I did is:
III3 = 1/1 Rr, III4 = 1/2 Rr, IV1 = (1/2*1/1*2/3=1/3)
III7=1/2 Rr, III8= 1/2 Rr, IV=(1/2*1/2*2/3=1/6)
IV1 x IV2 = 1/3*1/6*1/4 = 1/72.
The answer in the book is 2/35. Can somebody please explain where I went wrong?

Here is my attempt!
Generation III

III3 is rR
II3 is rR and therefore III4 is rR with probability $\frac{1}{2}$ and RR with probability $\frac{1}{2}$.
Just like III4, III7 and III8 are rR with probability $\frac{1}{2}$.

Generation IV
Let's start with IV1.

IV1 is rR if ...

III3 transmits the r allele (probability $\frac{1}{2}$)
III4 is rR (probability $\frac{1}{2}$) and transmits the r allele (probability $\frac{1}{2}$). The total probability is $\frac{1}{4}$.

However, we have to remove the probability that both parent transmit the r allele as we know IV1 is not rr. This probability is $\frac{1}{2} \frac{1}{4} = \frac{1}{8}$. So, in total, the probability of IV1 to be rR is $\frac{1}{2} + \frac{1}{4} - \frac{1}{8} = \frac{5}{8}$.

Now, IV2

IV2 is rR if ...

III7 is rR (probability $\frac{1}{2}$) and transmits the r allele (probability $\frac{1}{2}$) or if III8 is rR (probability $\frac{1}{2}$) and transmits the r allele (probability $\frac{1}{2}$).

However, we have to remove the probability that IV2 is rr as we know this is not the case. The total probability is therefore $\frac{1}{4} \frac{1}{4} - \frac{1}{16} = \frac{7}{16}$.

Generation V
Finally, we get to your question

[W]hat is the probability the offspring of IV1 x IV2 will show the recessive trait?

Both parents need to be rR which happen at probability $\frac{5}{8} \frac{7}{16} = \frac{35}{128}$ and both need to transmit the $r$ allele which happen with probability $\frac{1}{4}$. Hence the probability is $\frac{35}{512}$.


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Help in identifying an unknown Golden Worm/Larvae
Can anyone help me to recognize this type of species? Is it a clustered worms or clustered larvae? Location is in Bali, Indonesia. Recently this species is goes viral, but people here always link this species to a myth.
Thanks.

These are larvae of the so called fungus gnat of the order Diptera. Fungus gnats are small flying insects that look sort of like mosquitoes but they don’t bite. In fact, adult fungus gnats live only about 7-10 days and do not feed. It is the immature larval form that can cause damage to your plants.

Source: https://www.projectnoah.org/spottings/30766835/fullscreen
I see, i'm Balinese too, you know everything things were rare are linked to myth.

Welcome to SE Biology. It seems like you have identified the species but we prefer these answer to include a link and/or some photos that confirm the identification. You can edit the question to include these.


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I need help identifying a bug
Basically this tiny bug plopped on top of my laptop keyboard. And as much as I disdained bugs, this one didn't look like anything I've ever seen. It had something that resembled bits of a dandelion on its back, and its body seemed like half a moth/ whatever insect. After closer inspection, I thought it was just a dying moth, the thing on its back being clipped wings and its body cut in half... but when i tried to shove it off the keyboard with my pen, it jumped about a hundred times its width onto my wall - instantly. Tried to get a second picture but it jumped again/disappeared... no idea where it went, or what it was... Here's the picture I took, and a quick sketch of what it looked like.

What's your location?

This looks like an immature passionvine hopper (Scolypopa australis).  They are informally known as fluffy bums.

Source: http://ketenewplymouth.peoplesnetworknz.info/friends_of_te_henui/images/show/1486-nymphs-fluffy-bums-scolypopa-australis
This is am image of the adult stage from the Encyclopedia of Life site:

More information can be found at the Encyclopedia of Life link above.  It appears that their distribution may be only in Australia and New Zealand and I'm not sure where this photo was taken so take this information into consideration.


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Are all/most/any membranes comprised of lipids from the smooth ER?
I'm attending an introductory high school course to cell biology. Based on my understanding, lipids – the building blocks of membranes – are formed in the smooth ER. Are all/most/any membranes comprised of lipids that are formed in the smooth ER? If not, where do the lipids of membranes come from?

It sounds like we're mainly interested in phospholipids here, as they're the main component of cell membranes. Since your question didn't specify, we'll talk about Bacteria/Archaea and Eukarya separately
Bacteria/Archaea
Here, the answer is fairly intuitive. Bacteria and Archaea don't have endoplasmic reticulum, so they can't synthesize phospholipids in it. In this case, it seems like they create fatty acids directly from enzymes in the midst of the cytosol.
Eukarya
Here, the answer is a bit more complex. Fortunately, there are some good reviews about the topic that answer the question. Here, they talk about the entire phospholipid biosynthesis pathway and only mention the ER as an organelle, although it's worth noting that there are several sub-locations within the ER where specific groups are added. However, they fail to distinguish between rough and smooth. In another source, they mention not only the ER but also the mitochondria as having some ability to synthesize phospholipids. That's pretty cool, in my opinion.
TL;DR:
Bacteria and Archaea certainly don't rely on the smooth ER for lipid synthesis. In eukaryotes, there are several areas where lipids can be made but the smooth ER does seem to be the main source.


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Has autogamy been observed in any animals?
By my understanding, autogamy, i.e., reproduction that is sexual, but with both gametes contributed by the same individual, is not at all uncommon in the plant kingdom.
Does this also occur anywhere in the animal kingdom?

@kmm I appreciate the help! But your revision greatly changed the meaning of my question, including cases I wanted to exclude and vice versa.

Then I suppose I don't really understand your question. What do you mean "animals that have sex with themselves?"

@kmm is it not adequately elaborated on, explained, in the text body? If not I think the text is what may need further sharpening up!

Perhaps he means self-fertilization? https://en.wikipedia.org/wiki/Autogamy

Yes, there are some animals which are known to self-fertilize (although generally not exclusively).  For instance, among invertebrates some nematodes are known to use self fertilization, as discussed in this paper about its evolution.  Among vertebrates, it seems to be very rare, apparently known only only in a single genus of fish.

It sounds like you're referring to self-pollination. This is a specific subset of the larger category autogamy, in which two gametes from the same individual fuse.
It looks like this has been documented most completely in starving Paramecium, although Britannica seems to think it is common in invertebrates as well (without a source).
One source thinks that plants are the most successful example of autogamy because the development of several pollen tubes simultaneously allows the plant to carefully choose the fertilizing source, enabling it to select for genetic material that can mask the deleterious recessive alleles.

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Why EtBr migrate toward the opposite direction？
We known that DNA would run toward the positive electrode, because of they have negative electricity. then why EtBr migrate toward the opposite direction to DNA?
is because they have positive electricity?

EtBr runs the same direction as DNA. If it runs the wrong way, you probably have your red wires on top (mixed up)

Ethidium bromide itself is neutral in charge, however in aqueous environment it's a positive ion and it travels towards the negative electrode, opposite to DNA, as DNA is negatively charged and travels towards the positive electrode.
The thing is, it doesn't matter all that much. Whether you prepare a gel with EtBr added or you add EtBr to the electrophoresis buffer, it will instantly start intercalating the moment you insert your sample or start running the gel. The moment the electric current is applied, EtBr will indeed start migrating towards the negative electrode but some finite amount would have already intercalated into the DNA and it's going to be visible under UV only when bound to DNA. Keep that in mind that EtBr is a much smaller molecule and penetrates the gel easily, but will get trapped in between DNA base pairs if it happens to find some.
With that said, as one of the commenters pointed out, if your samples seem to have travelled the other way around, you have probably swapped the cables. The charge of the electrode depends on the charge applied by the source of electric current and if you mistake the cables, you will actually make the samples travel towards the opposite direction.

Negatively charged anions migrate towards the anode electrode during electrophoresis.  Likewise, positively charged cations migrate towards the cathode electrode in electrophoresis.  Neutral molecules, lacking any net charge whatsoever will remain immobilized in the loading wells.  The net charge on a molecule in an aqueous buffer depends on the both the molecular structure, and the pH of the buffer.  If you agree with all of these facts, then you have answered your own question.


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Can the theory of natural selection distinguish between two correlated phenotypic traits?
Consider the following two situations:

A species X has trait $T_1$ that is gradually selected for by some characteristic $E_1$ in some ecological niche but it turns out that the genes for $T_1$ also "turn on" genes for trait $T_2$ so that eventually species X with trait $T_1$ also have $T_2$. Then it turns out that $T_2$ is evolutionarily advantageous i.e it does help in increasing fitness because of some characteristic $E_2$ in that same ecological niche.
A species X has $T_1$ that is selected for by some characteristic $E_1$ in some ecological niche, this ecological niche also has characteristic $E_2$ that separately selects for $T_2$.

Both of these cases have as the end product $T_1$ and $T_2$ being advantageous for survival but in one case $T_2$ was selected for and in the other it's usefulness was accidental. What in the theory of natural selection distinguishes these two cases? To put things more bluntly, you are an evolutionary biologist and you are telling the standard story that corresponds to situation 2, how do you know (from the theory of natural selection) that we can discount situation 1?
I did a research project for my undergraduate research where I simulated mutations of cells in a petri dish and I know that mathematically these two cases can be disentangled because they lead to two different cluster size distributions with different scaling laws. As a physicist I know what to do but does a evolutionary biologist using theory of natural selection know what to do.
Update: The point is that in case 1 $E_1$ and $E_2$ could act at different times so that only $T_1$ is responsible for survival and $E_2$ while acting $T_2$ was completely useless for it's survival i.e other species disappeared not because they didn't have $T_2$ but because they didn't have $T_1$. Then a naive biologist could tell separate evolutionary stories assuming that $T_1$ and $T_2$ were selected for separately because when the biologist is observing the situation both $E_1$ and $E_2$ are present and $T_1$ and $T_2$ are present.  In other words, he or she would assume case 2 occured. In this case, random mutations and natural selection as told in science classes is completely useless because of $\textit{dynamics}$ in the environment and $\textit{correlations}$ that prevent mutations from being just random.
Why does this bother me? Well, because I hear evolutionary accounts that span hundreds of millions of years and it would seem simply applying the Darwinian story naively could make wrong predictions all over the place. I haven't seen people worry about this as they give evolutionary accounts for everything. From sexual behaviors to marketing.

I am not sure I understand the question. How is your question different from a classical correlation vs causation question in statistics?

Note by the way that you seem to confound the concepts of "environment" with the concept of "ecological niche". You might want to have a look at their definitions.

@Remi.b that may well be true that in my question I confound the two, but looking at the definition of "ecological niche" I think my question still runs through.

@Remi.b I can rephrase the question in terms of correlation vs causation. The simple story is that traits that correlate with survival or fitness are responsible for survival i.e they are selected for. But in case $1$ $T_2$ is correlated with survival or fitness a posteriori but is in fact not selected for.

So is your question "Are biologists aware of the causation vs correlation problem or are they noobs in statistics?" :)

@Remi.b they could be aware of it but ignore it. But I am really interested in people who apply evolutionary reasoning like evolutionary psychologists.

I am not sure why you talk about your interest in evolutionary psychologist. Note that evolutionary psychology is for the moment an extremely theoretical field with very little empirical testing.

mutations are not truly random nothing in the real world is, they are statistically random enough.

Are biologists aware of the causation vs correlation problem or are they noobs in statistics?

Evolutionary biologists tend to be pretty good statisticians. For historical consideration, Pearson is the father of the concept of correlation and was a biostatistician and Fisher is (one of) the father of evolutionary genetics and is also a famous statistician (invented the Fisher's exact test, t.test and Anova). Many of the modern developments in modern statistics were brought about by geneticists (incl. developments in HMM, ABC, FDR, etc...).
So, yes we are aware of the causation vs correlation problem.

In the theory of natural selection, can the two situations be disentangled especially when one is talking about evolutionary accounts that are on the order of hundreds of millions of years[?]

Just like in any other causation vs correlation problem, no it is not easy to disentangle the two. If the specific hypothesis put under testing is subject to experimental manipulation, then yes, it is often feasible to disentangle the two. Otherwise, in a purely observational study, one can logically reason and argue for one rather than another causality relationship but in essence, you cannot know in a purely observational study whether a correlation is representing a direct causation.
The follow-up question might then be

Is experimental manipulation feasible in evolutionary biology?

The answer is yes. Not for all questions though.
First there are evolution experiments. An evolution experiment is just like what is sounds like. You put a population in a controlled environment and let it evolve. Repeat the process many time to have a decent sample size. There are also many question of interest to evolutionary biology that can be studied through experimental manipulation (and not only observatory studies) that do not require an evolution experiment.
You seem to be particularly interested in the reconstruction of past evolutionary history of a lineage (evolution biology is much more than a 'historic' reconstruction of life on earth), I would like to highlight that in purely observation studies and in experimental studies not involving evolution experiments, there are plenty of methods to reconstruct past events. Consider for example the loss of genetic diversity at linked variants (selective sweep) caused by positive selection. If two traits are correlated through time (which is very hard to figure out in absence of good fossil records) or correlated over several species (consider having a look at phylogenetic contrasts methods and more modern version of inference of selection over phylogenies), then if selection occurred in a single of the two traits, you should expect to see a differential loss of heterozygosity among the genetic markers explaining ariance for one trait and for the other.

I am sure biologists are aware of the generic problem of causation vs correlation problem any one in the sciences is. You have merely diluted the force of my question to simply being about whether biologists have opened up books on statistics, I know they have. But that is not my question. In the theory of natural selection, can the two situations be disentangled especially when one is talking about evolutionary accounts that are on the order of hundreds of millions of years. How would one do that generically in the theory of natural selection.

Unless the selective pressure applied by $E_1$ and $E_2$ are applied at different times, it seems like the two scenarios you described are equivalent. In other words, if in both ecological niches, $E_1$ and $E_2$ were present from the start, and both $T_1$ and $T_2$ were present from the start, then absent other factors, the process and result are the same.
However, if you are saying that in the first scenario, $E_2$ was applied only after $E_1$ was selected for, then it is likely that $T_2$ was a genetic hitchhiker, i.e. it didn't provide any advantage before, but the niche has changed and now it provides an advantage. If this is what you're talking about, then you want to look into the concept of genetic drift. Basically, genetic drift is the random mutation of alleles. Genetic drift can lead to speciation if groups of the same species are separated by some sort of barrier to reproduction.
One way to determine if a gene is being actively selected for is to calculate the $K_a/K_s$ ratio which compares the rates of non-synonymous and synonymous substitutions, respectively.

In case 1, $T_2$ only appeared because a mutation caused $T_1$ so that $T_2$ is a hitchhicker and was not selected  for and so $E_2$ was applied after $E_1$. A naive post hoc evolutionary story would simply observe that $T_2$ is advantageous and so was selected for but this would be wrong. I know these can be disentangled mathematically but these sorts of stories are told about evolutionary processes that happened over billion of years where we might not have access to data that could disentangle these two situations. This is my worry. Has this been thought about?

"A naive post hoc evolutionary story would simply observe that T2 is advantageous and so was selected for but this would be wrong."
This wouldn't necessarily be wrong. T2 was in fact selected for, just at a later time than T1. So it sounds almost like you're after the relative time of emergence/selection of 2 traits? In that case, you could maybe build separate phylogenies for each gene/set of genes, and then compare branch times, but other than that, I'm not sure.

Yes relative time of emergence is everything!  Because in the first case it is possible for species $X$ to survive only because of $T_1$ while other species disappear. $T_2$ would emerge later on but it would serve no purpose in the competition because $E_2$ emerged in the environment and acted on $X$ much later on. A naive biologist would simply conclude that $T_2$ was selected for because of $E_2$ but that would be wrong. It would seem random mutations and natural selection is too simplistic. There can be correlations in mutations and dynamics in the environment

Ok, I understand now! It seems to me that there are some methods that exist to determine the relative age of certain segments of a genome based on how many/what type of mutations have been accumulated, but I am not familiar with these methods. Additionally, you may be able to tease out relative emergence by looking for other organisms that have $T_1$ but not $T_2$ (or vis versa), indicating that certain subsets of the population were exposed to $E_2$ while others were not. But this is getting beyond my expertise.
At least I finally figured out the proper mathematics formatting!

Firstly, I think that you should take a look at the genetic mechanisms behind convergent evolution.
In addition to the above statements, I would say that for your null hypothesis, you would need a situation where if there is a T1 then there is an E1 such that T1 positively regulates T2. Therefore, we can infer that T1 also has T2. I also believe that you can frame this statement using universal instantiation, if you are familiar with either logic or discrete mathematics.
For the second situation in your original question, we could say that there exists a T1 such that characteristic E1 and E2 could result in T2.
I prefer to use the language of logic such that we can build a mathematical model (and perhaps an estimate of all of the different combinations) by integrating the Ka/Ks ratio and the use of some sort of Bayesian analysis or graph theory representation to note the spread of genetic drift and an attempt to delineate the different effects that these mutations could have on phenotypes

As is obvious, I am not a biologist. Can what is being described in the comments and your answer be applied to evolutionary stories that occur on geological time scales ? That is to say, are these two cases  regularly disentangled before people claim what trait was selected for. I am hoping people don't just observe phenotypes and study ecological niches and then weave stories combining the two.

Possibly, I think. What I described is mainly mathematical, and I figured that since you are a physicist, you may know what I am talking about. I only say this because mathematical models in this area are still being developed and the usefulness of these models for biology are still being tested experimentally. I just outlined a more streamlined process to use the mathematical models and current experimental data to test possible disentanglement.

First selection does not occur at the species level. Scientist don't talk about a species going extinct due to the lack of a gene.
Second you seem to be confusing what evolution can "tell" with what scientists can tell. The spread of a gene is a statistical correlation occurrence, evolution cannot tell what gene causes a phenotype, genomes are selected for whole hog so to speak, (there are some rare exceptions). It is only through recombination that gene can be segregated, in your example it could be determined that T2 is only active when combined with T1 such situations are well known. indeed this is one of the hypothesis as to why various forms of sex/transfer evolved in the first place, to allow the decoupling and loss of disadvantageous genes.
Third entangled linkage and selective pressures are quite common many traits have multiple effects including counter effects and effects contingent on other genes. What you are describing is a regulatory or linked genes vs  independent genes. This is the norm for genetics and is extensively studied and is the reason genetics is not as easy as laymen think it is.Very few genes have only a single selective effect and control genes are quite common.
There is even investigation in the fact that un/successful genes are physically linked by and can effect the survival of other genes in the population just by being physically close to anther gene on the genome and thus likely to be passed on together even with recombination. Entire branches of genetics exist to study linkage.
In your own example there is no accidental usefulness, one is simply a linked or regulatory trait while in the other both are independent.  So to answer your question yes evolutionary biologist are quite aware of the issue.
What is told in a classroom, especially a basic classroom is a simplified more abstract version of what is known,  in your own field nobody is going to start teaching physics with quantum dynamics, or the relativistic effects on a normal trains mass, you start with simpler and somewhat outdated/incomplete equations until the students can grasp the basic concepts. You are not going to talk about Neutron diffraction with students before they understand what friction and mass are. In a description of the evolution of the avian respiratory system or the function of the human facial recognition system, linkage of individual genes is irrelevant, what is being discussed the dis/advantage or function of the phenotype NOT the genotype that brings them about.

I am not confusing what biologists can tell with what evolution can tell. In fact this is precisely why I asked the question, the point is when a biologists decides between the two cases does he or she use the theory of natural selection i.e random mutations and survival of the fittest or do they claim to use theory of natural selection but what is really doing the explanation is something else. From the answers it seems what is really doing the explanation is not theory of natural selection per se .

As to your physics analogy, no physics teacher would claim frictionless incline planes and massless pulleys describe the real world; they are presented as highly idealized simple models. On the other hand, the theory of natural selection is not described in school as a simplified abstract model and it seems to me there are professions that do not treat it as an simplified abstract model i.e evolutionary psychology, hence my confusion. Anyways I think I am getting the idea

no but they use them in class problems all the time, I'm just trying to explain why your teacher or a paper may not have described in the detail you want. Or to put it another way if I am describing a pulley system used to lift trains the gravitational pull the pulley exerts on the train is not worth worrying about. Everything you are taught in school is simplified.

As for what biologists do without an example I can't comment on what you think is happening, It is far too generalized and unclear. If you want to make another question and give an example and ask what is being talked about that's a great use for this site. any number of things could be going on everything from a bad source to  confusing phenotype with genotype to mistranslation, ect.

For examples Gad Saad a youtube personality and evolutionary biologist claims to study consumerism from an evolutionary perspective or people who speculate about the evolutionary origin of language. It seems to me that in these two examples the back bone of explanation is the simplified abstract model.


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What gives nerves their silver colour?
I always thought the silver colour specific to nerves was due to the myelin sheaths, but I've observed that unmyelinated C fibres display that same silvery appearance. Where does this colour come from? And can you distinguish myelinated from unmyelinated fibre bundles with the naked eye from their colour?

I don't know if I've heard "silver" as a color description for nerves of any type..white maybe in the context of white matter? Where are you seeing C fibers?

So I'm taking this from experiments done in animals. The spinal cord basically looks like a big, thick, silver straw (I always looked at the dorsal half, so including the dorsal columns which are Abeta fibres). I recently had a look at nerve around the splenic artery (which consists of C fibres almost exclusively). All these nerve to me look like silver shiny straws. I would love to attach some photos but I'm not sure that's appropriate...

Short answer
I think the whitish color is due to the outer layer of nerve bundles: the epineurium. This surrounds all nerves, whether they contain myelinated fibers, unmyelinated fibers, or both.
Background
Nerves are bundles of axons (Fig. 1). Whether the axons are myelinated or not, the gross anatomy is similar; axons within a nerve are bundled into fascicles and surrounded by perineurium. Those fascicles are again bundled up and surrounded by epineurium. It is this epineurium that you probably are seeing and it has a whitish appearance (Fig. 2).
The surface of a nerve therefore does not contain myelin; myelin is present around individual axons and is not exposed. Hence, whether a nerve contains myelinated axons, unmyelinated ones, or both will not determine its outward appearance.

Fig. 1. Anatomy of a nerve bundle. source: EasyNoteCards

Macroscopic view of a nerve targeted for epineurial repair. source: wikipedia

Ah that makes sense to me, thanks a lot for this detailed answer @AliceD !


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Have there ever been as many mammals as there are now?
I apologize for the weird question, but based on a Google search it looks like this topic hasn't been discussed before. I'm hoping that enough information about population biology is stored in the fossil record to answer this question.
Humans have wiped out a lot of animals in a very short time, but I realized that mammals might be doing very well.
First off, humans are mammals, and there are 7.6 billion of us. That's quite a lot. I don't believe any other animal species of our body size has such a large population.
Second, humans have pets. A lot of them. And they're almost all mammals. Everywhere we go we take our cats and dogs with us. Many of them become feral and multiply prolifically.
Third, our livestock. With the growth of human civilization came the growth of meat consumption, which, naturally, meant a lot more cattle. I think I read somewhere that cattle are contributing more to global warming than cars, through burping.
Lastly, and probably most importantly: rodents. Cats chased us everywhere because rats chased us everywhere. They thrived on the grain we grew and their population exploded to the point that they became a global pest, and possibly humanity's greatest enemy.
So, my hypothesis is that there are more mammals now than ever before in the history of life. Not in terms of species diversity, but in terms of headcount. If this is true, it would be remarkable, since the rest of the Animal Kingdom is currently suffering through a mass extinction.

Interesting question. At first, my knee-jerk answer was "yes". But then I saw you were talking about individuals, and not species. Humans have certainly skewed the numbers, favoring domesticated species, and eliminating others.

During the ice age, when there were many great plains, there must have been a staggering number of  prairie dogs, lemmings, gophers etc. I don't have time for an in-depth literature search but it appears that studies focus on biomass and less on numbers.

There can be perhaps 10 trillion rodents and bats on the planet, so the humans and livestock probably are small compared to a rainforest rodents and bats. The biggest bat colony is 40 million, they decline without unmanaged forests, can reach 4-10 bats per hectare, and the world population might normally be in 10s of billions, save for the use of pesticides and deforestation.
Here's a bit of maths to say that we have erased 1 trillion rodent habitats through monocultures and ploughing. Every cow and sheep field would have previously supported 10-20-50 times more rodents, and they aren't adapted for pesticides and ploughs.
37% of the world's land is farmed
Extent of total cultivated land in 2006: 1.5 billion hectares.
If there were 14 mammals per km2 of farmland, then we have displaced 20 billion mammals.
If the pristine habitats previously supported 1 rodent/mammal every 5m2, we would have destroyed the homes of 2000 mice,voles,shrews,squirrels and other mammals by hectare, that's 3000 Billion mammals (worst case scenario) due to monocultures and farming, and 1000 Billion in a best case scenario. Bangladesh rice farms and UK fields both are hostile to mammals.
A 20g mouse for 5m2 comes to the same as one human for 15 square kilometers. A mouse only needs a 3g of seeds/roots/beetles/snails per day to survive, that's about a kilo per year. "blue oak, interior live oak, and black oak respectively produce 2955, 1074, and 616 kg/ha of tree canopy" invertebrates provide 100-300kg/ha.
Perhaps we have erased 1 trillion mammals in the amazon alone.
https://www.worldatlas.com/articles/list-of-primates-by-population.html
Also we have depleted the fish stocks. It is reported that in medieval times, the seas heaved with incredible amounts of dolphins, whales and fish stocks, pristine seal and dolphin numbers could have been about 1 billion. Perhaps today it's about 1/4 of that.
If i had to bet all I own on your theory, I'd say it happened at another time in the previous 60mn years, probably not today.

It looks like this comes down to rodent population. I'm surprised the density can go as high as 10mice/m^2 in any large area. Source?

I had a hard time finding any sources that compare mouse density in woods to their density in farmland. But my intuition was always that mice benefitted from human expansion. We wiped out their big predators and left wide open row crops for them to munch on. This back-of-the-napkin calculation gives a ridiculously high mouse count for one agricultural region. Also, consider their introduction as invasives in places like NZ.

I was researching it a bit fast, I did mice m2 in and the first page i had was 10/m2 so i added that, I have edited it. sciencenordic.com/rodent-population-swings-remain-mystery
Sep 4, 2015  70 to 100 rodents for each 1000 m2 of forest floor in southern Norway. a cold country with slow growing forests and smaller tree seed harvests. primeval forests have heaps of dead wood everywhere and masses of seedfall.

I did a bit more research. I wouldn't say it's a certainty that more farmland means fewer rodents. This study found a maximum density of 379 rodents/ha in an Ethiopian wheat field. However, this other study found a maximum density of just 35 rodents/ha in an Ethiopian forest.

Of course, these are just two papers, and maybe another two papers will give the complete opposite result. In any case, do you have a source for the 2000 rodents/ha figure in your first post? I looked around, but never found a density that high.

there's an uphill climb to find references. To refactor your query into a clearly quantitative and thoroughly numerate study, is whether a family of mammals has ever been beyond the 1 trillion and 1/2 trillion figures. in nyc they dont know if there are 1/4 or many million rats. In rodent surveys they have to use traps with vole escapes because the voles die of hunger, and they run after mice with radio antennas in fields. they still dont know.

fields and irrigation, when arranged into en eischer rodent waterfall tower, dont use space and light efficiently to support a maximum of nesting sites for animals, we reduce complexity and age of all habitats and skew the mammal numbers towards smaller numbers of overgrazing large mammals. this is the best list of mammals i could find, no bats and rodents on there... i have to say i'm jammed on the rodent survey synopsis summery of current research on historical national mammal figures :) .https://en.wikipedia.org/wiki/Lists_of_organisms_by_population#Mammals_(Mammalia)

I think that in order to find out whether there as many mammals previously as there are right now, we would need to use procedures like DNA-seq and mTDNA sequencing to identify clusters of mammal extinction or the now extinct ancestors of current mammals.
Here are some relevant articles:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0003602
http://www.pnas.org/content/91/25/12336.short


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Pest on fenugreek
I need help identifying this pest on a fenugreek leaf. It is very common Maharashtra and Karnataka (India), and probably other states as well. Some of the leaves in the fenugreek bunches bought in the market have this kind of a distinct pattern. I am not able to pinpoint the exact orientation and shape/size of this organism on the leaf so I'll be glad to accept any help for that as well.

It is some kind of leaf miner, which should narrow the search. I am not sure what species.


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Is an animal's body height dependent on its environment?
Imagine the follwing situation: a newly born animal is brought into a small room. This room has no windows, but artifical light to imitate the sunlight. Furthermore, this light behaves like the sun, so that there are artificial nights and days in the room. The animal will be provided with food and water, too, so that it has enough nutrients to develop in a normal way. What will happen with the animal, when the room is so small, that it would limit the body height of the animal?
(One extreme example: an elephant, living in a normal sized room)
Would the growth of the animal be limited by some biological/biochemical mechanism? Or would the animal grow in a more or less normal way?
In summary, my question is: does the body height of an animal depent on its environment? If yes: how strong is this dependence?

The animal would grow normally to its natural height, but if limited, would continue to grow but become deformed. Do you have a specific reason for asking this?

@anongoodnurse Do you have any sources to read more about this? No special reason, I have just been curious about it. So no reason to panic: this is (of course) just a hypothetical situation!

Have you ever heard of the binding of feet in Chinese women? Hormones , and nutrition, etc.control growth, not space. Growth hormones + limited space = deformity. Sources, no. Any such experiment would be unethical, not to mention unhelpful.

@FlashTek do you think examples from anongoodnurse answers your question? If not, please explain why.

@anongoodnurse I did not really think about big experiments but rather observations about situations in which something like this has happend. Initially I thought, that the an animal in such a situation might release hormones which hamper growth hormones, so that the animal's growth will be limited.

Nature is red in tooth and claw. I can't see your situation occurring in nature. Likely the animal would die from starvation if confined to a small space unless in a lab for this particular, unethical, experiment. Even joey's outgrow their space...


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Oocyte cryopreservation: genes from three parents?
Recently, I've heard of something called Oocyte cryopreservation, where a (fertilized, I think) egg from a woman is extracted, frozen and later thawed and reinserted into the woman to delay pregnancy.
Now, this is just an idea, I don't know if this is actually possible, but can this frozen egg be implanted into a different woman, who isn't the original owner of the egg? If yes, whose genes would the child inherit? Would it get genes from all three parents, or just from the original owner of the sperm and egg?

In short: yes it is possible to donate an oocyte to another woman. This is typically done in assisted reproduction and combined with in vitro fertilization. The child would only inherit the genes from the donor oocyte and the sperm, as the genetic material is enclosed in the oocyte and sperm. There is no genetic contribution of the recipient.
You can find more information on the corresponding wikipedia page:
Egg donation


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Can crocodilians differentiate their offsprings from other young crocodiles?
I read that some species of crocodilians can take care of their young for as long as a year.
How do parents differentiate their offsprings from other young crocodiles? Smell, appearance, sound?

Crocodiles have very keen hearing and can hear their babies calling from inside their egg. I believe mother crocodiles recognize the sound of babies after they hatch also.


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Cell-level selection and inheritance of acquired mutations
I was reading about different levels of selection in Ridley's Evolution textbook (chapter on units of evolution) and saw that some organisms e.g. carrots are not Weismannist i.e. don't have separate somatic and germ lines and can make offspring with their somatic cells, and that this can in theory lead to cell-level selection because cell lines that outcompete others have a greater chance of leading to offspring and thus will be selected for. I think mutation that arises in a cell during the organism's lifetime and causes it to proliferate counts as an acquired mutation, but I've also read a lot that acquired mutations/characters aren't passed on a la Lamarck.
Is this a case where acquired mutations are passed on, and how does that fit with the usual concept that acquired characters aren't passed on? I know gene, individual, and kin selection are much more prevalent and Ridley says the cell-line selection idea is just theoretical, but what would this mean if it occurred?
Thanks :)

The first answer is correct - it resolves what you consider to be the Lamarckian dilemma. Is this a case where acquired mutations are passed on? Yes. Even in humans, in the germline, mutations accumulate slowly (or acquire mutations). This is not Lamarckian selection, however. There is no selection operating here.

In any reproductive event, we transmit new mutations to the offspring. In absence of cell-line selection, whether the mutation occurred during a meiosis or a mitosis is of little interest.
In absence of cell-line selection
A big difference between acquired mutations and Lamarck's acquired inheritance is that under Lamarck's view point, characters are being adaptive. Under Lamarck's view point, individual try to perform some action, stretch their muscles and other organs toward what is optimal for their needs and this phenotypic modification is being transmitted. The classical example is the example of giraffes. Giraffes stretch their neck trying to reach for high leaves, their neck is getting longer and their longer neck is being transmitted to their babies.
With acquired mutations, in absence of cell-line selection, there is no reason for adaptive mutations to be transmitted more often than non-adaptive one.
With cell-line selection
Now, if there is cell-line selection, beneficial mutations (beneficial at the cell level) are more often transmitted. The mutational process itself stil remain "random" (see Are mutations random?) but selection will increase the ratio of beneficial to deleterious mutations. Now, mutations that are beneficial at the cell level are not necessarily beneficial at the organism level. A typical example is cancer.


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20/20 vision translated to resolution
What resolution and or DPI would a TV or VR headset need to be to equal 20/20 vision? and 20/10? With even the 4K TV it does not seem as sharp as my own vision.

20/20 is a resolution. 4K not (but used wrongly as resolution)

@GiacomoCatenazzi You have it backwards.. 4K does refer to image resolution; specifically, it's the number of pixels running along the horizontal dimension of the image. Conversely, 20/20 vision does not refer to resolution, but instead, the clarity of the image. You can have a 4K resolution image that's considered to be 20/200 clarity. To generalize: 4K --> amount of information in the image; 20/20 --> how well that information can be discerned into something intelligible.

@Muze Respectfully speaking, your question is based on inaccurate information. Resolution and clarity describe two different features of an image; although related, the two don't so immediately translate into one another. Resolution = how much data the image contains (how large is the image) ; Clarity = how "clear" the objects are within the image.

@Charles: no. Number of pixels is not a resolution. It is just used wrongly for computers (and now also on televisions, but TV industry (content side) carefully never used resolution in such context (also because pixels was not a real thing). In any case it is already fading out (number of pixels), because it causes problems, now we are seeing things from much more diverse distances (phone, computer screen, television) as previously. You could use PPI (pixels per inch) as a resolution for screens and paper, or usually it is refereed by lines per angle unit.

@GiacomoCatenazzi A pixel can be used to describe nearly any image, not just what appears on TVs, computer screens, smartphones, etc.. From a mathematical & computer science perspective, if the image is represented as a dot matrix data structure, then a pixel is a point in the matrix. Most respectfully speaking, given your comments, I think you have a slightly incomplete understanding of what a pixel truly is, and I recommend you do some more reading. :)

@Charles: really. I know about what I'm speaking.You are oversimplifying a complex topic.Really: do not use pixel count as resolution! Do you know that pixel in CSS are not pixel as you mean it (retina display and printing). A pixel on screen has different colours (the subpixels), but on a photographic sensors such subpixels are pixels (so having just one colour ingormation). On printers we use "dots", because dots can be made of different size, and each colour have different resolution. The underling technology (and pixels) should not be taken into account on creating contents.

Let us continue this discussion in chat.

@Charles  I am interested in both of your answers.

@GiacomoCatenazzi Both point of views has merit and revise the question to be more broad.

Not really on-topic for here, but what sort of video are you playing with your 4K screen? Unless you actually have 4K video, it doesn't matter how many pixels you have. Also, what Giacomo is getting at is that the number of pixels is not the only key - also important is how close you are to the screen. The pixels on a stadium "jumbotron" are going to be huge compared to those on a phone or computer monitor, because they are meant to be viewed from a long distance. There's a big difference if you are up against your TV versus across the room.

Also, 20/20 vision is just a reference to human norms: 20/20 vision means you see an image 20 feet away with similar clarity to how a "normal" human sees an image 20 feet away.

To measure acuity, it's important to have a measure that considers visual space rather than physical world space (it doesn't make any sense to talk about "millimeters" because that says nothing about how far away the object is), so one would normally talk in terms of "degrees or arc" where 360 degrees is a whole field in all directions. Within degrees of arc, you can refer to "arcminutes" which are 1/60th of a degree of arc. If you could see everything in front of you, but nothing behind you, then you have 180 degrees of visual field in both horizontal and vertical dimensions (humans actually have a much smaller visual field than this), or 10,800 minutes of arc.
Your visual acuity greatly depends on where on the retina an image falls; the 'fovea' is the center of the retina where your vision is most sensitive. In the fovea, the maximum acuity is somewhere around 0.5-1.0 minutes of arc (see for example Rossi, E. A., & Roorda, A. (2010). The relationship between visual resolution and cone spacing in the human fovea. Nature neuroscience, 13(2), 156-157.), which corresponds nearly to cone density in the fovea.
A good "rule of thumb" (no pun intended, since we won't be using the thumb here...) is that the width of your fist at arms length is about 10 degrees of arc, your pinky finger is about 1 degree of arc. To get 0.5 arcminute resolution, then, you would need a screen the size of your fist (600 arcminutes) held at arms length to be 1200 pixels wide. Modern cellphones held at a moderate distance likely come near this limit, whereas TVs and monitors typically do not; however, you probably view your phone much closer than arms length and your TV much further.
Realistically, however, pixel counts far below this are sufficient for most scenes, because acuity measured this way is referring to the ability to separate points of light. In real natural vision, we aren't usually separating points of light, but rather organizing visual representations into salient objects, so the actual pixel density required to get a smooth image is less. Pixel limitations are more likely to be apparent when displaying text, since contrast is much higher with text than with natural scenes.

References
Rossi, E. A., & Roorda, A. (2010). The relationship between visual resolution and cone spacing in the human fovea. Nature neuroscience, 13(2), 156-157.


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Electrical field stimulation of neurons: what are commonly used stimulation protocols and which are physiological?
I am doing a labproject with primary mouse nerve cultures (hippocampus and midbrain) and part of the experiments involve performing electrical field stimulation on these neurons.
For now we have decided on three different types of stimulation:

1 Hz for 20 sec (20 action potentials)
50 Hz for 2 sec (100 action potentials)
20 Hz for 2 sec (40 action potentials) which my promoter said was commonly used

I have been looking for (but not finding) other commonly stimulation protocols, especially those with physiological levels.

Are the protocols I have chosen physiological or not (or under- or overstimulation) and why is this so? I assume neuronal subtype also might play a part in this.
Are there other commonly accepted paradigms for electrical field stimulation of neurons?
How can I stimulate my cells within physiological levels?

Any advice, explanation and or further references to find answers to these questions are appreciated!

I think this question is much too broad to answer here - you are better off consulting with people in your lab and reading the literature. Appropriate stimulus paradigms depend entirely on what you are trying to accomplish, and defining them as "physiological" is always going to be context-dependent.

I agree with @BryanKrause that your question is not specific enough. We would need to know what you want to accomplish. Furthermore, while someone may present an argument about what is physiological for the intact hippocampus in a living animal under certain conditions, it is not at all clear to me that any boundaries make sense for cultured neurons beyond perhaps extremely high frequencies (say >300Hz) applied for a prolonged period of time.


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How do cell signaling ensures time synchronization?
Let us suppose two cells A and B communicating with one another, I want to know how do cells ensure time synchronization while communicating. For instance, let us assume cell A sends a sequence '110'. Where '1' corresponds to dissemination of certain number of molecules, while '0' corresponds to no transmission of molecules. Now, cell B detects first '1', and then because of some delay in the reception of another '1', the sequence now received is '101'.
I want to know that how do cells ensure time synchronization?
Or because of very small distances over communication range, there is no need of it?

As far as I know, cells don't detect sequences like you're proposing (though of course, there could be exceptions). While cells can detect changes in signal over time, it's not as straightforward as on/off, and this is generally modeled in analog terms via complex sets of differential equations.

Look at, e.g. http://science.sciencemag.org/content/298/5596/1241 for some examples of how cells can respond to transient signals of different lengths

Maybe the more robust option for sending signals like "111" vs "110" is combinatorial regulation - multiple different types of molecules, so information is conveyed by seeing whether molecule X is high AND molecule Y is high, etc.

Sorry! But I can't understand your last comment, do you want to say that some type of AND gate is used here to doubly ensure the proper detection.


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What does reflected onto means in the text below?
The pleura lines the thoracic wall and diaphragm, where it is known as the parietal pleura. It is reflected onto the lung, where it is called the visceral pleura.

"Reflected" here describes the relationship between the continuous, but differently named parts of the pleura. The parietal pleura lines the chest wall and mediastinum (costal, cervical, mediastinal, and diaphragmatic areas marked in the image below). The visceral pleura covers the surface of the lungs (orange area below). There is a transition point at the root of the lung where the parietal pleura and visceral pleura meet. This transition is referred to typically as a reflection.
I think that the terminology is used to emphasize that the layers are continuous, but it is as if the parietal pleura bounces back off the body wall as visceral pleura.

Although not a particularly clear choice of words, because we usually connote "reflection" with light, in this case, "reflected" refers to how the parietal pleura folds back on itself from the inner chest walls and diaphragm to line the lungs.


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Do non-functional (‘junk’) protein sequences exist?
For DNA one can distinguish between

protein-coding DNA sequences, i.e. nucleic acid sequences inside DNA (vs. non-coding sequences)
DNA sequences that do not code for proteins but are transcribed into functional RNA
non-transcribed DNA sequences that have other (e.g. regulatory or structural) functions
non-transcribed and non-functional DNA sequences (‘junk DNA’)

The relative proportions of these seem to depend heavily on the organism and are only roughly known.

What I wonder is whether there are protein sequences (i.e. amino acid sequences inside a protein) that have no functional purpose.

A non-functional protein sequence might be a sequence that is neither effective to the outside (e.g. as a site for post-translational modification) nor to the inside (e.g. in folding). But even those parts of the protein might contribute structurally by their sheer presence and mass which is important when considering proteins not only as chemical but also as somehow mechanical devices. This might be called its structural purpose.
Assuming that each part of a protein has either a functional or only a structural purpose the question arises what the relative proportions of functional vs. only structural parts are.

Could your title be : "Do non-functional protein sequences actually exist?" (possibly without the "actually")? It seems like you are saying that surely all sequences have some function.

I have removed the word sequence as a qualifier for protein wherever what you are talking about is the physical entity — the product of translation of a mRNA — a protein. Further, the terminology you use is unfortunate because the term ‘functional’ is often used in contrast to structural. I have therefore added “junk” as an alternative. Finally, your question is unanswerable. If a protein exists, it is impossible to prove that has no function. I have added this as an answer, but I think your question should be withdrawn on that basis.

I'm afraid you distorted the spirit of my question which was intended to be explicitely about amino-acid sequences inside a protein, not about the protein as a whole.

Oh dear, that's unfortunate. David's answer does still apply somewhat to your actual question, but could focus more on things like disordered or unstructured loops in protein structures, I guess. This paper might be interesting : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882790/

Sorry about that. And I only just picked up your comment as you hadn't put an @David in so that I would be notified. I would still avoid the word "sequence" like the plague when talking about actual entities. The reason is that it emphasises the conceptual pattern, rather than the physical entity. If I understand it you are talking about linear portions of the chain of amino acids in actual synthesized proteins. If this is the case, it is also a difficult question, but in a different way, and worth asking. I can help you construct another question if you wish.

@David: I would be pleased!

I suggest a question with the title: "Are there functionless stretches of amino acids in proteins?" And the question follows in the next comment. If it fits the bill (perhaps with changes) you could mount it and we could modify this question and cross reference them.

Suggestion for Question: The variation in amino acid sequence of the same protein in different species indicates that at certain positions different shapes or even polarity are possible. Nevertheless an amino acids at such positions may be necessary for the overall structure of the protein. In contrast I am interested to know about stretches of several (perhaps six or more) successive amino acids — tails or loops, perhaps — that evidence suggests to be unnecessary for the protein. Do these exist and, if so, what proportion of the proteome do they constitute?

This question is unanswerable as, if a protein exists as a physical entity in a cell it is possible to demonstrate it has a functional or structural role, but it is logically impossible to demonstrate it has no such role. The best one can say is that “it has no known function (role)”.
That said, in the course of evolution following gene duplication and divergence it is theoretically possible that on the way to acquiring a new functional role there is a stage at which a protein has no such role. One might be able to identify such proteins in a gene family like the globins by examining a range of species, as has been done for the globin genes. I am not aware of any such studies.


text:
What is the difference between hilum of the lung and root of the lung?
In my book they describe root of the lung like this:
In the region of vertebrae TV to TVII, the mediastinal pleura refects off the mediastinum as a tubular, sleeve-like covering for structures (i.e., airway, vessels, nerves, lym-phatics) that pass between the lung and mediastinum. This sleeve-like covering, and the structures it contains, forms the root of the lung.
And hilum of the lung like this:
The root joins the medial surface of the lung at an area referred to as the hilum of the lung. Here, the mediastinal pleura is continuous with the visceral pleura.
I dont see the difference between Root and hilum.
Can somebody please help me out?

Short answer: Hilum is an area(has only 2 dimensions) where as root is a body( has 3 dimensions).

The root of lung is a short broad pedicle connecting the medial surface of the lung with the mediastinum. It consists of structures entering and leaving the lung at hilum. The root of lung is surrounded by a tubular sheath derived from the mediastinal pleura.

and

The hilum is the area on the mediastinal surface of the lung through which structures enter or leave the lung.

Source: pg no 239
Consider the following image( edited by myself):
If the cylinder is root of lung then lateral opening(blue) is hilum.

The region bounded( within the limits of pleural membrane) by those two planes is root of lung and the area bounded by the lateral plane is hilum.

Any reason for downvote so I may improve?

I didn't downvote, but I think you could mention which structures does the root consist of.

The root of the lung is region of the mediastinal surface of the lung that lies between T5 and T7, it consist of the mediastinal and visceral pleura reflecting over the structures entering or leaving the lungs at the hilum like a sleeve.

Welcome to Biology.SE! It isn't clear to me as a non-expert in anatomy that this adds anything to the existing answer and reads more like a comment on that answer. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!

Root of of lung is a pedicle which connects medial surface of the lung with the mediastinum and lies at the level of 5,6,7 thoracic vertebrae.
It consists of structures going in and out through a triangular depression called hilum.

Welcome Prince Kumar. Please take our [tour] and refer to the [help] as and when for guidance as to our ways. This is a perfectly reasonable answer, but we'd like you to add references as a rule to support the info. Enjoy Biology.


text:
Insect ID Montreal, Qc Canada
I found this bug in my kitchen, in front of my oven.
It has wings and moves quite slowly on the ground.
I can provide additional pictures if required.
Can somebody tell me what it is?

I have found an article on a local website that seems to say this is a carpet beetle even though it's written bedbug right bellow it.
http://www.exterminationmontrealbedbugs.com/insects/

As a general hint: everyone on the internet calls every small insect a bedbug, every brown spider a brown recluse, and every 3 leaved plant poison ivy. There is a TON of misinformation and wrongfully ID's species rampant all over the internet. Stick to well cited or reliable sources (e.g., .edu or .gov, websites, science journals, etc.). In general,  TRUST NO ONE 0.o

Dermestidae, Reesa vespulae; wasp nest dermestid
http://pestcontrolcanada.com/5965-2/

Also, I find long-winded explanations of species IDs to be annoying. When the question is "what is this species?" the answer is two words.

Respectfully speaking, your proposed ID is not correct. I suggest you explore the genus Attagenus.

Let us continue this discussion in chat.

https://farm4.staticflickr.com/3253/2597399688_b6ca9e1370.jpg

I agree that it appears to be a Dermestid of some kind, but I'm not a beetle pro, and so I'm not going to weigh in on the specific ID.  Sometimes family is good enough, in my experience.  I merely want to say that in my experience, commercial pest control websites are not places I would look to for accurate identification information.  I'm sure they try hard, and some of them may have people on staff who know their business, but all too many simply cut and paste posters and photos from other locations, without regard for accuracy.  The common "Spider ID" poster that pops up in the US, which features Australian species, is a frequent source of irritation for me.


text:
Identify this tree from Nepal
This is a picture of a tree in Nepal. Can somebody identify it?

Do you have some more picture of the leafes? Will be hard to identify the tree solely based on the bark

I have uploaded photo of leaf.

The leaves on the top left have different veins than the leaf from the photo, Are they from the same tree?


text:
Geographic regions as subpopulations/demes
I am developing a computational simulation for DNA barcoding. One of the parameters in my simulation is the number of subpopulation/demes, which I label as $K$. Most studies that use DNA barcodes tend to focus on a single geographic region.
My question is: is it valid to presume that a single geographic region is equivalent to a single subpopulation/deme?
For example, if the focus was on cichlids of Lake Malawi, would it be a safe assumption that Lake Malawi comprises a single subpopulation/deme?
Eventually, I would also like to incorporate migration rates into my simulation, but these are very difficult to estimate without accurate data on $F_{ST}$.
Any insight would be most helpful and is warmly welcomed.

For simulating DNA barcoding, it is valid to presume that a single geographic region is equivalent to a single subpopulation. Although there do occur cases where one or two nucleotides differ at the same location, that is rare, and these few differences would still cluster together in any analysis of barcode data.

In terms of developing a simulation (simulations need not be perfect), over 50,000 specimens that I personally barcoded, I virtually never saw differences at the same location, and most data in BOLD are from single locations. "Region" in BOLD most often = single site. http://rstb.royalsocietypublishing.org/content/371/1702/20160025

Thank Karl! Based on your advice then, I am thinking that a user of my finished simulation could simply set the number of demes (K) to be equal to the number of sampling sites. Other more-involved options include using the software program STRUCTURE (Pritchard et al., 2000) to determine K using a Bayesian framework.

Yes, I agree. Sampling in BOLD is supposed to be geographically diverse. But it is common to have a single individual barcoded. Sometimes however, hundreds were sampled at the same site, and these were almost always identical. When the sampling was designed for barcoding, sites are usually at the extremes of species distributions, and these almost always differ. In this case, sites are not regions like "Virginia", but places where a collector stoped the car and collected. I have heard of "STRUCTURE", but have not used it. It sounds good though.

It is impossible to answer your question in the general sense. Yes, detailed population structure may matter. It very much depends upon what your question is and what parameter space you are willing to answer but it is possible that assuming panmixis would be unrealistic.
Note that accurate data on $F_{ST}$ won't suffice to estimate migration rate $m$.
Note also that many simulation platform already exist and you might not have to reinvent the wheel (see Sequence evolution simulation tool).

Thanks! I am not aware of any DNA barcoding studies that estimate migration rate; however an isolation-by-distance assumption would be required given population subdivision into demes.


text:
Are there differences between the activation proteins of Eukaryotes and those of Prokaryotes
I'm in BIO 203 (for reference to my skill level), and I noticed the textbook makes a whole section out of transcriptional activator proteins, their function and applications in eukaryotes, but in prokaryotes the term "activator protein" is used only once when mentioning the lac operon.
Are they the same type of activator proteins? Do they employ the same mechanisms?

In general transcription activators are transcription factors. These are very different in eukaryotes although some families share similar domains (e.g. two component signalization). I recommend you read through these two chapters to get a more complete overview on the differences.
https://www.ncbi.nlm.nih.gov/books/NBK21683/
https://www.ncbi.nlm.nih.gov/books/NBK21572/

As it stands your answer does not explain how these are different, and the two separate chapters you cite do not make such a comparison. For your answer to be useful you need to explain brielfy in what way they are different.


text:
DNA replication and combination

"Each gamete is genetically unique because the DNA of the parent cell is shuffled before the cell divides. This helps ensure that the new organisms formed as a result of sexual reproduction are also unique."

Then why do we say that the DNA of the parent influences the characteristics of the child while the DNA of the child is formed as a combination of shuffled up nitrogenous and phosphate bases?

Welcome to SE Biology. Please provide a citation for your quotation.

To explain it briefly:
Lets take a human as example, you are diploid and you have a pair of 23 chromosomes (= total 46) and the sex chromosomes which I will exclude for this explanation.
Your gamete is haploid and has therefore only one of the two paired chromosomes. So for every chromosome pair there are 2 possible chromosomes. So in total you have 223 possibilites to arrange chromosomes. The gamete from the sexual mating partner also has 223 possibilites to arrange chromosomes. So in total a new diploid organism has (223)x(223) possibilites. So unique.
However, it is always the chromosomes of the parents. So yes, parents influence the children because the genetic information of the children can be found in one of the two parents.
Furthermore you have recombination, but you already asked another question about this. So I will not expand this answer.
There are relevant articles in Wikipedia on genetic recombination and meiosis that I would recommend.

Thank you for your contribution. I have reset your programming-style powers in html superscript tags and replaced * by x for general readability. I have also rewritten your reference links in a way that it is clear what they refer to.

Parents influens children's characters because the shuffeling (crossing over)  changes only few genes present on the parent chromosome and also these changed gene peices are also parental so actually we recieve a non parental chromosome (generated by shuffling)but the genes present on it are still parental..  Hope this helps


text:
Insect identification - Possible grasshopper or grass beetle
We found a small insect on our window and we cannot decide whether it is a type of grasshopper or grass beetle. It doesn't seem to want to fly, but was on a first floor bedroom window, and walks slowly and has a strong grip on the window and petri dish. We live on the outskirts of a town in Essex, UK and it could have come from a field, but they are on the other side of the house. It is a small brown insect (the main body is approximately 2cm long) with 6 legs, and the back 2 legs seem to bigger than the others.

Neither beetle nor grasshopper, it is a hemipteran, Coreidae. Leptoglossus occidentalis or
Western Conifer Seed Bug.  https://www.britishbugs.org.uk/heteroptera/Coreidae/leptoglossus_occidentalis.html

This idenification looks good. Insects of this genus seem to have  variable spine arragements on their femurs. I'd like to know more about that.


text:
Why do universal recipients (AB blood group) not react to antibodies in the blood of O-group donors?
While studying compatible blood groups, I found that we only consider the antigens on red blood cells (RBCs) and not the antibodies present in blood plasma. For example

“an AB blood group person can receive blood from persons of any blood group as there are
  already both antigens, A and B, on the RBCs.”

But why don’t we consider the antibodies already present in the plasma from people with different blood groups?
For example, the O blood group has both anti-A and anti-B antibodies. If this blood is given to an AB person who has antigens A and B, do the antibodies of O not react with the antigens of AB?  Or, in other words, how is a person with the AB blood group a universal recipient if he has both antigens(A,B) in the blood, which can react with antibodies(anti-A and anti-B) present in indiduals of other blood groups (A, O, B)?

Always remember that plasma is not given while blood transfusion. So if you are giving only RBC of O blood group to the person having AB Blood group it will not react.

Although I answered this question, an older similar question has just surfaced for some reason. (The answer there is also more comprehensive than mine, and some comments more authoratitive.) I therefore flag this as a duplicate and have deleted my answer. (I may add something to the older question.)


text:
If a tortoise lost its shell, would it be naked or homeless?
We often call a snail's shell 'house'. But there are also naked snails (=slug).
What about tortoises? Is their shell like a house or an important part of their body? If a tortoise lost its shell, would it be naked or homeless?

The shell of a tortoise is physically attached to the rest of the skeletal structure. That being said, it's simply not possible for a tortoise (or snail, though, for slightly different reasons) to leave its shell.

If a tortoise lost its shell, would it be naked or homeless?

It would be both naked & homeless, as well as dead.

That’s a great picture. Where is it from?

@canadianer I thought so too! I obtained the image from DK, however, it appears to be widely used throughout the web, so I'm not sure if that's the original source.

Thanks. I’d love to see how the skeleton moves to retract the head inside the shell.


text:
How didn't large, highly active dinosaurs overheat?
The cube-square law seems to be the deciding factor when it comes to biological heat management. Small organisms with large surface areas relative to their volumes, like mice, need fast heartbeats and huge energy consumption relative to their size to keep themselves warm. Large organisms like elephants with small surface areas relative to their volumes need slow metabolisms and fairly little energy consumption relative to their size to keep from overheating.
But, dinosaurs. Most research seems to indicate they were basically warm-blooded (yes, that wording really bothers me too, but research as recent as 2015 states that they seem to lean decidedly toward warm-bloodedness, though they are technically somewhere in between). Modern-day creatures of that size tend to divide neatly depending on whether they live on land or in water, with the former being fairly inactive and herbivorous and the latter sometimes able to support the metabolic needs of predation by having water to help disperse the heat.
Dinosaurs, though, are an exception. Many of the fiercer predators were large, highly-active land-dwellers, three conditions that are mutually exclusive in modern organisms. How was this possible?

There has been a long debate whether dinosaurs were ectotherms or endotherms but  most of the recent studies (hypotheses)1 show that they were endotherms. In one of the most promising recent studies (in 2011), a technique called clumped-isotope thermometry2 (which is based on a reaction involving the bond between carbon and oxygen; and used in paleoclimate reconstruction) is applied to bioapatite (a form of calcium phosphate in bones and teeth) which acts like a thermometer.

The nature of the physiology and thermal regulation of the nonavian dinosaurs is the subject of debate. Previously, arguments have been made for both endothermic and ectothermic metabolisms based on differing methodologies. Here, we used clumped isotope thermometry to determine body temperatures from the fossilized teeth of large Jurassic sauropods. Our data indicate body temperatures of 36 to 38°C, which are similar to most modern mammals. This temperature range is 4 to 7°C lower than predicted by a model that showed scaling of dinosaur body temperature with mass, which could indicate that sauropods had mechanisms to prevent excessively high body temperatures being reached due to their gigantic size.
Dinosaur Body Temperatures Determined from Isotopic (13C-18O) Ordering in Fossil Biominerals
Robert A. Eagle, Thomas Tütken, Taylor S. Martin, Aradhna K. Tripati, Henry C. Fricke, Melissa Connely, Richard L. Cifelli, John M. Eiler
http://science.sciencemag.org/content/early/2011/06/22/science.1206196
(emphasis mine)

However, a study as of 2014 claims that dinosaurs were mesothermic3 (meaning the blood runs neither hot nor cold, a thermoregulatory strategy intermediate to cold-blooded ectotherms and warm-blooded endotherms) based on the metabolic rates of dinosaurs by looking at changes in body size as animals grew from birth to adults.

In early depictions, dinosaurs lumbered slowly, dragging their tails. More recently, we have imagined them lifting their tails and running. The question boils down to whether dinosaurs had energetic systems closer to those of rapidly metabolizing mammals and birds, or to those of slower reptiles that do not internally regulate their body temperature. However, determining the metabolic rate of extinct organisms is no easy task. Grady et al. analyzed a huge data set on growth rate in both extinct and living species, using a method that considers body temperature and body size. Dinosaur metabolism seems to have been neither fast nor slow, but somewhere in the middle—so, dinosaurs did not fully regulate their internal temperature but they were also not entirely at the whim of the environment; neither slow goliaths nor supercharged reptiles.
Evidence for mesothermy in dinosaurs
John M. Grady1,*, Brian J. Enquist2,3, Eva Dettweiler-Robinson1, Natalie A. Wright1, Felisa A. Smith1
http://science.sciencemag.org/content/344/6189/1268
(emphasis mine)

As we covered the thermoregulation system of dinosaurs, we can start with the question "How didn't large dinosaurs overheat?". As explained above, whether they were endothermic or mesothermic, dinosaurs had mechanisms to regulate their internal temperature not to overheat. There are theories that say that some larger dinosaurs relied on shade and dense flora to keep cool or they might have migrated due to seasonal changes. Other theories claim that they used large surface area organs (like long necks and tails) as a heat radiator4.
One of the most plausible explanations is that large dinosaurs displayed tachymetabolism. Tachymetabolic animals have high resting metabolic rates, usually resulting in endothermy and homeothermy. Further explanation of how big tachymetabolic dinosaurs coped with high heat loads5:

BIG TACHYMETABOLIC DINOSAURS WOULD HAVE COOKED IN THE HEAT
Myth: Because tachymetabolic rates scale to W0.75, while surface area scales to W0.67, it is almost universally believed that big endotherms suffer serious heat stress in tropical climes. Big dinosaurs, sauropods especially, should have had low metabolic rates to avoid this dire fate (Martin, 1979; Regal and Gans, 1980; Spotila, 1980; Reid, 1984; Schmidt-Nielsen, 1984; Carroll. 1988; Alexander. 1989; Prothero, 1989: Russell, 1989). Alternately. tachymetabolic sauropods needed well developed cooling systems (Bakker. 1980, 1986).

Figure 5 This plot shows the time it takes high level endotherms to overheat if they store all internal heat production and exclude external heat by allowing their body temperature to rise to maximum tolerable levels. The mass range approximates that of adult dinosaurs (including lagosuchians), with the highest masses of mammals also indicated: note that giant endothermic dinosaurs would have been more resistant to overheating than giant mammals! Energy storage capacity is in kcal assuming a 6-8°C rise in body temperature (up to 46.5°C), with 0.83 kcal/kg stored for each 1°C rise in body temperature; total active metabolic rates are either 2.0 times endothermic standard energy production/bout, or only 1.3 times normal standard metabolic rates due to suppressed levels of activity and/or standard metabolic rates. The results are in good agreement with thermal tolerances observed among large tropical endotherms.

  Reality: This is a major misconception (Costanzo and Paul. 1978; Paul, 1988a. 1990a). Many tropical mammals have reached from 1 to 20 tonnes, but no classic reptiles have done so, exactly opposite the predicted pattern. Elephants lack well developed evaporative cooling systems. Elephants living in treeless habitats do not drop dead from heat stroke, even in the most dangerous conditions of an extremely hot drought when it is not possible to dump excess heat by radiation or evaporative cooling in the first place, and shade is not available. Instead, large bull elephants have the highest survival rates under such circumstances, again opposite the predicted pattern (Owen-Smith, 1988). Field biologists have long known that endotherms from 100 kg on up use a classic thermal strategy in which their great mass is used to store a relatively low rate of internal heat production for most or all of the day, body temperatures are allowed to rise 3-10°C, and water loss is kept to a minimum (Schmidt-Nielsen et al., 1957; Taylor. 1969, 1970. 1972: Gordon. 1972; Finch and Rohertshaw, 1979: Schmidt-Nielsen. 1984). The built up heat is then unloaded into the cool night sky. This makes large endotherms practically invulnerable to over-heating under the harshest conditions, small endotherms must seek refuge or quickly die from heat stroke or dehydration. The large size of dinosaurs may have been an adaptation for better coping with high heat loads with a tachymetabolic level of heat production (Figure 5).

References:
1. The Evidence for Endothermy in Dinosaurs -
 Top Ten Hypotheses http://www.ucmp.berkeley.edu/diapsids/endothermy.html
2. Paleoclimate reconstruction using carbonate clumped isotope thermometry
(John M.Eiler) https://www.sciencedirect.com/science/article/pii/S027737911100268X
3. Why Dinosaurs Were Like Tuna, Great Whites, and Echidnas http://phenomena.nationalgeographic.com/2014/06/12/dinosaurs-tuna-great-whites-echidnas/
4. Sauropod Necks: Are They Really for Heat Loss?
(Donald M. Henderson)
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0077108
5. Dinosaur Studies - Commemorating the 150th Anniversary of Richard Owen's Dinosauria (By L. B. Halstead)

Further readings (supporting above theories or with different theories):

GEOL 104 Dinosaurs: A Natural History - University of Maryland -
Department of Geology -
https://www.geol.umd.edu/~tholtz/G104/lectures/104endo.html
Body Temperatures in Dinosaurs: What Can Growth Curves Tell Us?
(Eva Maria Griebeler)
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0074317
Ecology and Behaviour of Mesozoic Reptiles (by John L. Cloudsley-Thompson)
Dinosaur Paleobiology (by Stephen L. Brusatte)
The Dinosauria (edited by David B. Weishampel, Peter Dodson, Halszka Osmólska)
The Complete Dinosaur (edited by James Orville Farlow, M. K. Brett-Surman)
Encyclopedia of Dinosaurs (edited by Philip J. Currie, Kevin Padian)
Tyrannosauroid integument reveals conflicting patterns of gigantism and feather evolution (Phil R. Bell, Nicolás E. Campione, W. Scott Persons IV, Philip J. Currie, Peter L. Larson, Darren H. Tanke, Robert T. Bakker) - http://rsbl.royalsocietypublishing.org/content/13/6/20170092
Dinosaurs used nasal passages to keep brains cool - https://phys.org/news/2015-10-dinosaurs-nasal-passages-brains-cool.html