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Determining how much energy a plant takes in?
I asked a question on WorldBuilding.SE, "Are diamond berries possible?".
This led to asking a question on Chemistry.SE about the amount of energy required to burn a 1 ct. diamond (−6.527kJ).
The helpful commenter on WB.SE said that a plant would roughly require three times this amount of energy to essentially reverse the process through some biological means to create the diamond berry.  And that I would need to know the "wattage input" of various plants to compare with my hypothetical plant.
Is there a way to arrive at how much energy various plants take in?
Also any other related information from a biological perspective would be helpful.

Just a speculation for whether diamond berries could exist or not. This is not an answer for "what is the energy uptake rate of plants" because the actual question tends to be "whether a plant can gather enough energy to form diamonds". For energy uptake rate of plants please see MCM's answer.
Even though enthalpy of formation is same as heat required for destruction, burning a diamond is much easier than creating it (I presume it is easier to generate high temperature compared to high pressure). Natural diamond requires both high pressure and temperature to form. Synthetic diamonds are made by chemical vapour deposition; that also requires high temperature. Such high energies cannot be produced by any known organism (requires devices like arc furnace), and moreover at these temperatures the biological structure will disintegrate.
However there is one possibility of diamond berries; the berries would not be solid diamond though. A plant could be growing in an area where there are a lot of nanodiamonds (meteorite rocks) which could be bioaccumulated in the berries. Living organisms do accumulate nanoparticles [1,2]. There have been studies on biological application and effects of nanodiamonds too [3,4]. However these would not look lustrous like bigger diamonds. Xylem vessels in trees have a mean diameter of 30-40µm; it may be possible that the plant can take up bigger sized diamond particles. Density of diamond is ~3g/cm3 — three times that of water and it would require thrice the force required for water to get diamond to the destination.
For a spherical diamond of diameter 20µm:
Cross sectional Area = 314.15 µm2
Volume = 3351 µm3
Mass = 3×3351×10-12 ≅ 10-8 g
Gravitational force on the diamond = 9.8×10-8 ≅ 10-7 N
Pressure required to counteract gravity = 10-7/314.15×10-12 ≅ 3.18×102 Pa

However, I am not sure if that much of pressure can be generated within a vessel and whether small particles can be lifted like this.
There is another possibility that bigger diamonds are encapsulated by living tissue (not the fruits of course).

What I think would be a rough estimate (ignoring the physical/thermal requirements for diamond creation) TL;DR -- It's about 68W/m2 given the caveats below. Also:
Disclaimer: This is the best way I could think of to figure it out. It is a rough estimate only, and your level of desired precision will introduce more complicated calculations than the ones I've done. Not all of the calculations I performed are explicitly necessary, but were simply the best way for me to wrap my head around it at the time and may be incorrect!
Since plants are mostly glucose and water you could find the net glucose content of the plant (which will vary greatly -- but let's give a rough estimate of 90% as an average). So if you have a 10kg plant, ~1kg of the mass will be a mixture of cellulose, starch, and other stuff.
For the sake of ease, let's ignore the other stuff and focus on the cellulose and starch which we'll say makes up the 1kg. Both Cellulose and Starch are Glucose configurations, so what we have is 1kg of Glucose.
According to Wikipedia the net amount of energy a plant devotes to biomass construction/CO2 fixation is 3-6%, and the Gibbs Free Energy conversion of CO2 to Glucose is 114kcal. If I've done my math correctly that means a mole of CO2 to Glucose for a typical plant takes 2280kcal (or about what I burn in a day as a 6'4" man).
So, how many moles of Glucose is in our 1kg Glucose plant mass? The molecular mass of Glucose is 180.16g/mol. 1kg/180.16g/mol = 5.55 moles of Glucose. We don't need to know how many moles of CO2 we started with because we're not limited there; the atmosphere provides all the CO2 we could ask for. We just know that we have 5.55 moles of Glucose, and it took 12654kcal of energy to convert however many moles of CO2 into that many moles of Glucose.
That 12654kcal is also equivalent to 52944.34kJ of energy. Now, the solar constant is ~1.36kW/m2 ... or (1360J/s)/m2. So, how much area of your hypothetical plant is exposed to the Sun? A square-meter isn't an unreasonable amount for larger houseplants, so let's just work with that.
52944.34kJ / 1.36kW = 38929.66s = 648.82min = 10.8 hours' worth of Sun exposure to produce 1kg of plant mass. Some species of Bamboo can grow 91cm/day, but I couldn't find a source for density... but nearly 3-feet of bamboo could definitely weigh 1kg.
Sooooooo... Plants "take-in" 1.36kW/m2 when exposed to sunlight. How large the plant's area is will determine how much energy it takes in overall. How much energy a plant devotes to producing its mass is about 3-6%... or about 68 Joules every second (68 Watts using 5%) for a large plant with 1m2 exposed area.
Your 1ct diamond would take just over a minute and a half if 100% of the plant's mass-growing resources went into it.
Of course, that seems really fast. The important assumptions are that the plant is in direct sunlight, is not limited by other factors (Nitrogen is actually a major rate-of-growth limiter, as-is Phosphorous), halts all other growth-oriented metabolic activity to do so, and the metabolic processes for the conversion other carbon forms to Diamond was 100% efficient with the energy the plant demarcated for growth.
In reality about the only potentially "true" assumption from that list is that it's completely possible to have a plant with 1m2 of surface area exposed to sunlight. Everything else will be a fraction of what the working assumptions are.

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How exactly do birds get drunk eating fruit? Fermentation should be anaerobic
The Washington Post article Drunk birds are causing havoc in a Minnesota town. Police say they’ll sober up soon. describes birds becoming intoxicated after eating berries:

“The Gilbert Police Department has received several reports of birds that appear to be ‘under the influence’ flying into windows, cars and acting confused,” Police Chief Ty Techar wrote in a statement Tuesday. An early frost meant that berries had fermented earlier than usual, he explained, and birds were eating them and getting drunk.
Incidents around town involving intoxicated birds appear to be more prevalent than in past years, Techar added, because many have not yet migrated south. “It appears that some birds are getting a little more ‘tipsy’ than normal,” he wrote. “Generally, younger birds’ livers cannot handle the toxins as efficiently as more mature birds.”

A few supporting videos:

ABC TV: Drunk birds are flying into windows, cars
TIME: Drunk Birds Are Flying High In Gilbert, Minnesota | TIME

Is the fermentation happening to the berries while on the tree or on the ground as the police suggest, or is it really after being ingested by the birds? How is an anaerobic environment produced for fermentation into alcohol but not subsequent conversion to vinegar?
Humans are a clever species, on par with some birds. They are known to collect the berries and ferment them first before ingesting, and will forage for a trap to let gas escape but keep the oxygen out. Have birds found a better way?
 Source

The insides of fruits are relatively anaerobic environments. Natural fermentation, as in berries that get birds intoxicated, is primarily from yeast, and it seems most likely that humans recognized this process before intentionally encouraging fermentation of anything. Natural fermentation reaching high ethanol concentrations occurs especially when berries high in sugar are frozen and then thawed.

Dudley, R. (2004). Ethanol, fruit ripening, and the historical origins of human alcoholism in primate frugivory. Integrative and comparative biology, 44(4), 315-323.
Fitzgerald, S. D., Sullivan, J. M., & Everson, R. J. (1990). Suspected ethanol toxicosis in two wild cedar waxwings. Avian Diseases, 488-490.

Interesting! I usually think of the inside of fruit as sterile, but maybe that's not exactly the case. Sounds like the basis of a new question!

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How many genes per 23 chromosomes in human genome?
It is estimated that humans have between 20,000 and 25,000 genes. Every person has two copies of each gene, one inherited from each parent.
There are 46 chromosomes, half from the mother, half from the father.
Does this mean that there are
a) approximately 20-25,000 genes on the 23 chromosomes inherited from the mother, and 20-25,000 genes on the 23 chromosomes inherited from the father, or
b) approximately 10-12,500 genes on the 23 chromosomes inherited from the mother, and 10-12,5000 genes on the 23 chromosomes inherited from the father?

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I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

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Answer A is correct!
The human genome has around 20,000 genes. In both, diploid and haploid chromosome-count, the gene-count stays the same; grown humans have 2 alleles per gene in most of their cells, which is considered 'diploid'. Gametes are haploid.
Willyard, C., Expanded human gene tally reignites debate. Nature, 2018. 558(7710): p. 354-355.

Please don't encourage posting of "homework" questions which do not show research efforts.

I did spend quite a lot of time searching for a clear answer to this question. I couldn't find one and that's why I posted the question here.

The aim of stack exchange is to develop an extended topic-related FAQ. I did not find this question here. As this is a natural question that I remember from my own study-years, I really don't care if this is homework; as long as it serves a purpose on the site / for google, it should always be accepted.

This isn't 'homework' by the way. I'm studying on my own, for myself. PS @KaPy3141 : thank you.

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How many hairs per sq. cm. (or inch) do hamsters have on average?
How many hairs per square centimeter (or inch) do common pet hamsters (Mesocricetus auratus or Phodopus sungorus) have on average?
I thought this would be easy to find by googling, but the best I've been able to find is this 1986 article, which isn't very clear in answering the question.

According to Paul et al. (2007), shaved fur patches of male Siberian and Syrian hamsters had a mass of about 12 mg/cm2 dorsally and 3 mg/cm2  ventrally.
This search give me the page.

Fig 1 from Paul et al. (2007) compares mass of fur growth across time for 2 groups exposed to differing lengths of daylight (long, LD, and short, SD) to examine winter fur adaptation.

Paul, M.J., George, N.T., Zucker, I. and Butler, M.P., 2007. Photoperiodic and hormonal influences on fur density and regrowth in two hamster species. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 293(6), pp.R2363-R2369.

Thank you, but it looks like the results are in mass of hair per cm^2. It would help if I had data for what was the mass of 1 hair (or 1,000 hairs), but unfortunately, I don't have such data.

@Enivid calculating the mass of a single hair is less time consuming than counting all the hairs, and it's certainly something you could try yourself to add such info to this post. Any secondary or post-secondary school will have a balance that I'm sure they'd let you use. I'd recommend a digital model


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Does the fact cordyceps mostly affect insects have something to do with chitin being polysaccharide?
This is just a conjecture of mine based on those observations:

Fungus seems to be very good at attacking tough chains of sugars like cellulose and starch.
insects are covered by Chitin, a polysaccharide.
cordyceps only attacks arthropods and in rare instances other fungus. Both arthropods and fungus have chitin in their body.

My initial guess was no but there might actually be some evidence for this. For example, host-switching between fungus and insects apparently happens within relatively small taxa of cordyceps, suggesting that host specialization is not too dramatic.
Moreover, there does seem to be some evidence that chitin is a relatively important metabolic input for at least one cordyceps species.
I don't know that we could say that chitin is the thing that allows the host switching or that it is the most important nutrient for cordyceps or anything like that, but it looks like it at least helps.
It's worth noting that ecological characteristics may play at least as large of a role. The phylogenetic study noted that host switching likely occurred from cicada nymphs (which hibernate underground) to truffles (which have their main mass underground), so it's possibly just an opportunistic jump in the soil environment.
It would be interesting to see if there is a "chitin sensor" mechanism in cordyceps that yields a signal to cordyceps that there is a host to invade. But I don't think that I saw anything that suggests that (though it's far from unprecedented in biology).


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What is more dangerous, exotoxins or endotoxins?
Since gram- negative bacteria tends to cause disease to human and they mostly produce endotoxins. Does this mean that endotoxin is more dangerous than exotoxin? and if that so why?

No. Exotoxins are more dangerous than endotoxins. endotoxins are made up of lipopolysaccharides, but exotoxins are made up of proteins, of which most are enzymes. due to the catalytic nature of enzymes, even a small amount of exotoxins can be dangerous (even micrograms of exotoxins can be dangerous).
[differences between exotoxins and endotoxins]1


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What are minerals (other than zinc) that the human body cannot store
It is known that zinc is an essential mineral that the body cannot store.
What are other minerals, especially metals, that the body cannot store?
(other than water-soluble vitamins such as vitamin B and C)
Sincere thanks.

Essential "minerals", i.e., metal cations are magnesium, zinc, iron, potassium, sodium, manganese, molybdenum, selenium, cobalt, copper and even calcium, as we lose a tiny amount of it through urine and sweat. They are all "stored" in some way, but only temporally, so some amount has to be taken up daily. It would show only weeks later, however, if you have a deficiency.
Wikipedia adds phosphorus and iodine but they are not metals.

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Do you know what this black spider-like insect is?

I have encountered these insects before, but I always assumed them to be spiders even though I always noticed they have 6 legs, as an exception. But slowly with time I ended up observing them more. One day I almost stepped on one of them, but thankfully didn't crush it and that was the day I realized they may not be spiders at all, Because I felt like I had stepped on a thorn or something. These insects are 6 legged and that rules them out as spiders but can't be sure. They don't seem to have distinguishable spinneret. If they don't belong to spider species then it is possible that the spider-like appearance is mostly a camouflage and a single spike on their back would be a defensive measure. They don't seem to behave aggressive like spiders.
I live in a rural area, State of Odisha, India

Related: https://biology.stackexchange.com/questions/87848/what-bug-is-this-manchester-uk/87853

that sort of makes sense, I need to observe and research those more....

They normally have 8 legs. You can see it is missing its second-to-front left leg.

thanks to autotomy


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Can one derive COVID-19 risk from a cheap consumer genetic test like 23andme?
Studies have found genes associated with a significantly higher risk of severe COVID-19, some of them claiming it to be 1.6 times the general risk.
They mention genes at markers such as rs35044562, rs1129183, rs679599192 to be significant.
Can people use the raw data from a consumer-grade genetic test like 23andMe to assess their risk, at least theoretically? The raw data has many gaps and the markers and their positions may not be included in the data. Can one then look at markers at positions close by, or at other markers? Does a more rare genotype imply higher risk?
Articles

https://www.nature.com/articles/s41586-020-2818-3
https://www.biorxiv.org/content/10.1101/2020.11.02.365551v1.full.pdf

I would strongly recommend talking to a genetic counselor about any results found on a genetic test, whether it be about COVID-19 susceptibility or anything else. Also, please keep in mind that personal medical questions and health advice are off-topic on Biology.SE. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice. This question is generic, so I'm not going to vote to close it, but I just wanted to make you aware in case you were planning on doing this yourself.

I suppose the answer is 'theoretically yes, but don't trust the results much'.
The 23andme genotyping array is very useful for ancestry testing, but much less useful for clinical diagnostics. I have worked in the past for Genomics England (an arm of the NHS in the U.K. which performs genetic diagnostics for rare disease). There, the samples were sequenced to very high coverage and underwent extremely stringent quality control checks which were being constantly updated. If you want to interpret a variant in a clinical sense, you have to very sure that you get the right genotype.
I believe that the details of how 23andme performs its variant calling and quality control are proprietary and therefore I would never trust their variant calls for any kind of clinical diagnostics, and neither would any clinician I know. This doesn't mean 23andme results are invalid - they are very useful and pretty accurate for testing ancestry, but they are not valid for clinical diagnostics. If your risk calculations hinges upon a few SNPs of relatively large effect size (such as BRCA), then you want to be very sure you make the correct variant call. You simply do not get this assurance with 23andme.
Secondly, like you mention, many of the SNPs you refer to aren't covered by the 23andme array. The effect size of a particular SNP on a trait is calculated for that specific SNP only. Extrapolating the effect size for one SNP in a gene to another, nearby, SNP in the same gene is likely to give you innaccurate results. In fact, the same SNP in the same gene can have pretty different effects in different people (https://febs.onlinelibrary.wiley.com/doi/pdf/10.1111/febs.14080 caused by the environment, pleiotropy).

Curious as to why this was downvoted?

No idea. It's exactly the sort of answer this type of question needs.


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Do slime mold expand or multiply?
After reading about slime mold I was wondering, do slime mold simply expand outwards or multiply?
e.g. if I put 100 grams of slime mold in 1 location, will it expand to say, 2 locations, and have the 1st location with 80 grams left, and 2nd location with 20 grams (i.e total 100 grams), or is it that they multiply; 1st location still 100 grams, and 2nd location with 20 grams?

It is difficult to understand your question expressed in grams and locations. I suggest a question about multiplication would be better expressed in number of cells in the first instance, with the size of the cells a second parameter.

The answer is that they will do either or both, depending on conditions: this is one of the things that has caused complex systems scientists to be so interested in things like using slime molds in modeling optimization problems.
In good nutritional conditions, the cells will happily multiply. At the same time, they will flow and reshape themselves to spread and migrate in search of food when nutrients are not uniform.

Thanks a lot! Any idea about the growth rate (e.g. multiplications)? I was trying to find it but couldn't. If you are familiar with any paper/sources that would be great!

I haven't personally worked with it, just heard about it from colleagues who wanted to do slime-mold computing.


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Can Taq polymerase be stored with PCR primers?
I don't think it's possible for TAQ to be stored with the primers, but I'm not sure. This storage wouldn't be long-term (a few days, or a week at most). Thoughts?

I have kept PCR stock solutions containing everything except DNA template for days to weeks at 4°C, and it works fine, at least for screening purposes (say, E. coli colony PCR or purified plasmid templates).

@gaspanic -20C would be ideal, though, especially for the dNTPs.

@MattDMo dNTPs are perfectly stable for months at 4°C, see for example here and here. I always keep an aliquot of my dNTP stock solution at 4°C both for convenience, but also to avoid repeated freeze-thaw cycles.

@gaspanic that's good to know, thanks

Yes, this is perfectly fine. Many companies sell PCR Master Mixes (granted, without primers):

Thermo Fisher
Sigma-Aldrich
BioRad
Promega
Qiagen

If you choose to make your own, make sure it's stored at -20°C, and be sure to aliquot it so it's not going to be subjected to multiple freeze/thaw cycles. Obviously you should mix it well before aliquoting, but even after thawing I would vortex it to make sure all of the components are well-mixed. Make a 2X master mix, and adjust to a final 1X concentration in the PCR tube with your DNA sample and nuclease-free H2O.


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What is the probability of virus undergoing a specific dangerous mutation?
Non-biologist here so apologies if the question is violating too many of the community standards for asking a question in the forum.
What got me thinking was imagining how much more terrifying the current situation would have been if the COVID virus had very long incubation period of something like 6 months and a higher mortality rate with the same rate of spread. By the time someone realizes that a virus is spreading, it would have already infected the entire planet. If it has a very high mortality rate as well, wouldn't that pretty much mean the end of the world?
My question is, what is the probability that this can happen? For example, what is the probability that a virus starts spreading with an incubation period and mortality rate of HIV but has the spread rate of COVID?

HIV and covid are two very different viruses, which behave diferently in how they are transmitted, and how they replicate themselves within cells. You may want to read this answer, to get a bit more background on how viruses lifestyles differ: https://biology.stackexchange.com/a/97324/59521

Thank you for the response, I understand your point about the HIV virus and how it's very different from the COVID one, and maybe I should have phrased my question differently, but my question was along the lines of, "what is the probability that a virus like the COVID virus mutating so that it has properties like a really long incubation time and more mortality rate"

Questions of probability are very hard to answer with any amount of confidence. I think a related question that is easier to answer may be: What are the viral traits that underlie measured variables like incubation time and mortality rate? Are there constraints imposed on the trade-off between these traits?

HIV and SARS-CoV-2 are two very different viruses in terms of how the are transmitted, how they replicate within the cells, how they interact with the immune system, etc. All of these aspects of a virus existence are highly adapted to assure virus survival (otherwise this virus quickly goes extinct). The ongoing mutations do help a virus to adapt to somewhat changing environment, but do not radically change it.
Thus, a virus that combines a long incubation period of HIV while being highly contagious as SARS-CoV-2, would be a completely new species, different from either of these two viruses in its genetic makeup, lifestyle, etc. It could take millions of years of evolution for such species to develop. Moreover, such a development is unlikely, since such a virus would exterminate its host, thus becoming extinct itself. The scenario that is more plausible is that of Ebola - a virus that exists as relatively harmless in some animals, and can evolve within them, but is highly lethal when it spills to humans, which results in deadly out breaks that quickly end. Probability of such a nightmare scenario is as small as a probability of the world ending due to a black hole generated in Big Hadron Collider or huge meteorite striking the Earth - while it cannot be mathematically excluded, it is too small to account for it in our daily lives (as compared to other dangers).

That's good to know. Thanks for the explanation. I can sleep a bit better at night.


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Could two different pairs of humans generate the same child
What I mean is this. Take male A, female A, male B, female B. Is it possible for the pair of male A x female A generate a child that is genetically identical to a child from the possible children from the pair male B x female B? Assuming neither of the four are related in any way. In simple terms, take me, for example: could my genetic code be generated from a different mother and a different father that my mother and father? Would the answer change if one of the parents is the same (say, male A x female A versus male A x female B)?

What do you mean by 'genetically identical'?

Well, say, two people with the same genetic code. Like twins, for example. Except not from the same parents.

'Genetic code' isn't really a term that means anything. It sounds like I am being pedantic, but it terminology is very important for understanding. 'Genetic code' could mean either the same sequence of base pairs or the same sequence of codons. Which do you mean? And is there a specific reason why you are asking this question? Knowing this might help give a better answer, since sometimes the questions are based on a false understanding of the science.

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I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Forensic DNA analysis is essentially based on the fact that such coincidence cannot happen.
More precisely, the comparison between the DNA is done on multiple genetic locations, and the probabilities are evaluated that such a coincidence happen by chance. The standart use includes 13 locations, which is sufficient to confirm the identity beyond reasonable doubt:
Upon collection, the cells' DNA is extracted,
 and 13 genomic locations that vary among
 individuals are assessed to confirm suspects or exonerate those that are
 innocent.

This is to say that there is always a non-zero probability that the DNA of two different persons (even coming from the same pair of parents) are identical on all the 13 loci, but it is unreasonable to consider that such an event happens, given the human population size.


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Do stem cells have no epigenome?
Till now I thought that embryonic stem cells have no epigenome as they are pluripotent. (I thought that since epigenome is what gives a cell its identity, no cellular identity means no epigenome) I saw something similar to this on this Wikipedia page. After fertilization, the paternal and maternal genomes are demethylated in order to erase their epigenetic signatures and acquire totipotency..
Other sources mention 'reset' in place of 'erase'.
This paper rather suggests that stem cells do have an epigenome. Specifically, genes associated with self-renewal are silenced, while cell-type-specific genes undergo transcriptional activation during differentiation..
I am not very literate in biology, please excuse me if I made a mistake.

So there are a couple of things to bear in mind.

pluripotent does not mean that all genes are active. It means that the stem cells have the ability to form different cell types. However, it still needs to keep the cellular programme of a neuron for example silent. So the epigenome is still present to keep other cell type programmes silent until there is a transition.

DNA methylation is not the only source of epigenetics. Active and inactive genes also correspond to particular post translational modifications on tails of histone proteins. In the cell, DNA is wrapped around histones to form what is known as chromatin.

Hope that is a starting point to answer your question


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Melatonin production, sleep, and "cyan light"; how might this finding be possible?
The BBC News article Cyan colour hidden ingredient in sleep describes research that suggests melatonin levels as measured in saliva could be affected by the presence or absence of cyan color in a displayed screen, even when the color balance was adjusted so that the difference was not visibly perceptible.

The colour cyan - between green and blue - is a hidden factor in encouraging or preventing sleep, according to biologists.
University of Manchester researchers say higher levels of cyan keep people awake, while reducing cyan is associated with helping sleep.
The impact was felt even if colour changes were not visible to the eye. (emphasis added)
The researchers want to produce devices for computer screens and phones that could increase or decrease cyan levels.

Is cyan going to keep you awake?

I am guessing that this even possible because color perception comes through the sensitivity of three (or four?) color channels and so two different spectra can appear to be the same color. An example might be that a green wavelength might appear to be the same color as the mixture of a blue and a yellow wavelength if properly adjusted.
But if the two stimuli are adjusted to have the same or similar mix of signals in the individual's color receptors, how might the melatonin production still be affected?
edit: According to Wikipedia, monochromatic light would have a wavelength in the range of 490 to 520 nm, and if you wanted to create a visual impression of cyan, you'd use a mixture of Green and Blue channels:
Wavelength    490–520 nm
Hex triplet   #00FFFF
sRGBB         (r, g, b)   (0, 255, 255)

Melatonin production is in response to photoreceptors in the eye, in part, the same photoreceptors in rods and cones that process and transmit information about the wavelength of light (eventually) to the visual cortex for vision. However, @uhoh was right to wonder whether there might be a separate receptor input for melatonin production.
There is an additional opsin (photosensitive protein), found in the ganglion cells rather than the rods and cones, that is sufficient for responding to light and causing the production of melatonin by the pineal gland (mediated by the suprachiasmatic nucleus of the hypothalamus). Processing of light signals by the circadian system is quite separate from processing by the visual system. This is discussed briefly in Chapter 47 of Kandel's Principles of Neural Science, but you can read more about it in this review.
The pathways involved in receiving and processing light as an input to the circadian system were discovered relatively recently. Consider that the optic tract was discovered in the 3rd or 4th century BC, and the retinohypothalamictract was discovered in 1971.

Thanks! As in everything else in biology, the closer one looks, the more complicated (or at least complex) it turns out to be.

I am guessing that this even possible because color perception comes through the sensitivity of three (or four?) color channels and so two different spectra can appear to be the same color.

While this can happen, this is probably not what the article is referring to.

But if the two stimuli are adjusted to have the same or similar mix of signals in the individual's color receptors, how might the melatonin production still be affected?

I would guess that the caveat here is "visible to the naked eye" -- that is, the viewers didn't consciously perceive the cyan color. That doesn't mean that your eye didn't transmit its presence, as vision is the most "processed" sense we have. The screen you're reading this on is made up of RGB pixels on a scale small enough that your brain blends them together to construct an image made of the average color of the pixels.
It's very possible that there could be some cyan colors mixed in right now, but not in high enough concentrations for your brain to average them out into something you consciously "see".
For the experiment it's probably something similar: The cyan was there and picked up by the eyes, but the post-eye processing performed by the brain filtered it out from conscious view. That, however, doesn't mean it can't impact other portions of the brain. You still perceived it, it might still have an effect elsewhere, but your brain just isn't presenting it to you as "important" information.

I'm wondering if the receptors that lead to this response are completely separate from those used for vision. That might be a good avenue to explore.

@uhoh that's an excellent thing to wonder. Good instincts!


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What are the sources of molecular hydrogen in human breath?
In the BBC News article CES 2019: Tech preview of the expo's hottest new gadgets there is a new product that one can use to measure the hydrogen in ones breath, and this is supposed to have some connection to diet:

By contrast, FoodMarble's Aire measures the hydrogen in your breath and combines this with a log of what you have eaten, to warn you of foods you should avoid and possible substitutions.
Aire is designed to discover which foods are being passed to the large intestine without being fully digested

There also exist air quality monitor chips that measure both TVOC (total volatile organic compounds) and "eCO2", where "eCO2" is really a measurement of H2 in the air, and via some electronic algorithm uses it to calculate the expected rate that people are exhaling CO2.
Question: Both of these are examples of interpreting the presence of molecular hydrogen as having some indication that we are alive, breathing and eating. Here I would like to understand the sources of hydrogen in human breath, and how that hydrogen makes it from source to breath.
potentially related: Where does molecular hydrogen in the atmosphere come from?

They explain on their website.

@canadianer Thanks! I'm not sure how to judge the validity of foodmarble.com could you consider writing a short answer and quoting that page? That way other readers can comment and possibly add more information or other sources.

If I have some free time I will. They do link to scientific articles on that website. The gist of it is that this isn’t new technology (all they’ve claimed to have done is make it available to consumers) and it is based on hydrogen fermentation by bacteria in the gut.

@user1136 thank you for the link, and I see what you mean. Pardon me a moment, I'm going to brush my teeth now... ;-)

Hydrogen in breath arises from normal intestinal bacteria, mainly in the colon, which break down (ferment) the undigested nutrients that have passed through the small intestine. Hydrogen is absorbed from the intestine into the blood and exhaled via the lungs.
Conditions in which intestinal bacteria produce hydrogen:

Normal digestion in which soluble dietary fiber is not digested in the small intestine. Examples of soluble fiber: beta-glucan (in oats and barley), pectin (in apples) fructo-oligosaccharides (in red onions), raffinose (in beans), etc.
Lactose intolerance in which lactose remains undigested due to lack of the enzyme lactase (gas is produced mainly after ingesting milk)
Fructose malabsorption in which fructose absorption is reduced due to lack of a certain molecule in the intestinal lining (gas is produced after eating foods high in fructose: apples, pears, honey, agave, etc.)
Sucrose intolerance due to lack of the enzyme that digests sucrose
Small intestinal bacterial overgrowth (SIBO) due to various malabsorptive conditions

Hydrogen breath test is an established method for diagnosing various intestinal disorders. It includes drinking a solution high in certain substance (lactose, fructose..., depending on which disorder is expected) and measuring hydrogen in the exhaled air.
To properly interpret the results of a hydrogen test you need to consider the time in which hydrogen appears in breath after ingestion of a certain substance.
Food Marble provides a relatively thin explanation of their breath test. The question is if this test can distinguish between the hydrogen produced during normal digestion of the soluble fiber and hydrogen produced in the mentioned intestinal disorders.
Business Insider made a review of FoodMarble in which they mention some other reviews...In summary: it's not proven reliable, yet.

Wow, this is a real surprise! Thank you for taking the time to explain all of this and source well.  It looks like the rises are of order tens of ppm, so it's not a profound amount of gas.

The breath tests in hospitals are established and considered reliable, but the results need to be explained by a gastroenterologist. BreathMarble does measure hydrogen, but it is not clear how reliably you can explain the results.

yep I understand. Until now I had no idea of the order of magnitude of the amount, ppt? %? This is very small compared to what I first imagined.

Most of hydrogen goes out of the intestine at the back side... https://en.wikipedia.org/wiki/Flatulence


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Why do soil bacteria produce nitrous oxide as a result of anhydrous ammonia fertilizer application?
The NPR article and 4 minute audio news item Can Anyone, Even Walmart, Stem The Heat-Trapping Flood Of Nitrogen On Farms? discusses unexpected contributions of greenhouse gasses from the manufacture of consumer goods. One example is bread, or agricultural products in general, and part of this is the anhydrous ammonia used in fertilizer.
Carbon dioxide seems to be a bi-product of the manufacture, but nitrous oxide a more potent greenhouse gas is produced by bacteria in the soil as a result of application of ammonia.

Manufacturing nitrogen fertilizer is energy-intensive, burning lots of fossil fuels and releasing carbon dioxide. What's just as damaging, and perhaps even more so, is what happens when it's spread on a field. Bacteria feed on it and release a super-powerful greenhouse gas called nitrous oxide.
These bacteria are naturally present in the soil, says Philip Robertson, a researcher at Michigan State University, "but once they get exposed to nitrogen fertilizer, they really light up" and pump out nitrous oxide.

Question: Is it common for most soil bacteria to make significant quantities of nitrous oxide after ammonia is added, or is there only a small subset of bacteria present in soil that might do this? Also, what is the metabolic pathway in this case? Is this a waste product from "eating" ammonia, or something more complicated/subtle?

below: Anhydrous ammonia tanks in a newly planted wheat field. Walmart has promised big cuts in emissions of greenhouse gases. To meet that goal, though, the giant retailer may have to persuade farmers to use less fertilizer. It won't be easy. TheBusman/Getty Images. From here.

@GerardoFurtado I see, but my question is about nitrous oxide N${}_2$O and not nitric oxide NO.

@GerardoFurtado I understand what you mean - thanks! Also I've just changed my comment above - sorry about that.

@GerardoFurtado after a quick skim of the discussion and conclusion sections, I can see that this is in no way going to be an easy question to answer. Yikes! :-)

Addressing the first part of your question:

Is it common for most soil bacteria to make significant quantities of
  nitrous oxide after ammonia is added, or is there only a small subset
  of bacteria present in soil that might do this?

No, not all soil bacteria can oxidize ammonia. According to wiki:

The oxidation of ammonia into nitrite is performed by two groups of
  organisms, ammonia-oxidizing bacteria (AOB) and ammonia-oxidizing
  archaea (AOA).

The role of archaea in the soil nitrogen cycle is not well-known yet, although it could be greater than that of bacteria. On the other hand, the role and metabolism of AOB are more or less studied.
The process of ammonia-oxidizing is also called nitrification and AOB sometimes referred as nitrifying bacteria. The most known bacteria genera from this group are Methylomonas, Nitrosococcus, Nitrosomonas and Nitrosospira. I think the most studied species is Nitrosomonas europaea Winogradsky 1892.
For reference see: Arp DJ, Sayavedra-Soto LA, Hommes NG. Molecular biology and biochemistry of ammonia oxidation by Nitrosomonas europaea. Arch. Microbiol. 178 (2002) 250-5.
The second part of the question:

What is the metabolic pathway in this case?

Although, the metabolic pathways vary in different genera, let's look at ammonia metabolism in N. europea.
In the simplest case, it is a two-step process.
According to KEGG:
Step 1. The enzyme ammonia monooxygenase converts ammonia to hydroxylamine. The enzyme contains copper, iron and possibly zinc. It requires two electrons, which are derived indirectly from the quinone pool via a membrane-bound donor. The reaction is:
NH3 + a reduced acceptor + O2 = NH2OH + an acceptor + H2O

Step 2. The enzyme hydroxylamine dehydrogenase converts hydroxylamine to nitrite. This reaction requires specialized cytochrome as an acceptor of electrons. The reaction is:
NH2OH + H2O + 4 ferricytochrome c = NO2 + 4 ferrocytochrome c + 5 H+

While nitrite is the main product, the enzyme from N. europaea can produce nitric oxide as well. Therefore Step 2 can produce nitric oxide (NO). In this case, additional mechanisms of converting NO to NO2 are involved.
Further destiny of released nitrite can be different. In one process it could be oxidized by different microorganisms (bacteria, archaea) to nitrate (NO3) which could be consumed by plants or washed out to deeper horizons with water. In another case, nitrite, nitric oxide and nitrate could be involved in process of denitrification. During this process, a group of denitrifying organisms (bacteria, archaea and fungi) consume nitrogenous compounds and reduce them to nitrogen (N2), which can escape to the atmosphere. This process can occur through different metabolic pathways mainly with aid of reductases like nitric oxide reductase. One of the possible intermediate product of such pathways is a nitrous oxide (NO2). If N2O escapes from cells we can observe a resale of nitrous oxide from soil.
Let's return to your first question, and particularly to the part where you ask about significant amounts of nitrous oxide.
First of all, nitrification is a natural process and is a part of the nitrogen cycle. Some organisms fixate nitrogen and convert it to ammonia, some oxidize ammonia to nitrous compounds and some of them reduce it back to nitrogen. It occurs everywhere virtually in all terrestrial and water biocenoses. In a healthy ecosystem, the inflow of nitrogen is theoretically equal to the outflow (with temporal deposition in trophic chains). In such natural conditions, the release of nitrous oxide should be neglectable.
The situation changes significantly when we add an ammonia to soil artificially as a fertilizer. The main problem is that we break an equilibrium between nitrogen fixation, nitrification and denitrification. The second big problem is that an ammonia is toxic for most organisms, so we can alter microbiome. In such case, we can expect an excess of products of nitrification and improper denitrification with exaggerated levels of released nitrous oxide. The actual proportions vary significantly depending on both biotic and abiotic conditions, therefore it is difficult to predict real levels of nitrous oxide released without in situ examination.
P.S. sorry for possible bad writing.

Very interesting and informative answer! I will take a closer look in the morning, thank you!

Well that was quite a long morning! Nonetheless thank you very much for your answer! Just fyi I've asked a related question in Earth Science SE: How can agricultural ammonia lead to PM2.5 production in the atmosphere?

if I give you a can of anhydrous ammonia, and I drop in a match, it will blow up, yielding nitrous oxides.
it is an exothermic energy releasing reaction.
bacteria figured this out, and use this same chemical reaction, albeit with more steps, to derive their own energy, and therefore drive their own matabolism.
like the way a marshmallow (sugar) will burn, our bodies have figured out how to burn sugar without heat and yield ATP, certain bacteria do the same, but with ammonia. the nitrous oxides are then converted into nitrites by other bacteria, and finally to nitrate by yet other bacteria. And finally, some of the nitrates go into the plants, while others, get turned back into nitrogen, like when bitrate in gunpowder explodes (cool!)
this is called "nitrification" as some people in the comments have said.
google the nitrogen cycle if you havent already. it is very fascinating.

Can you be a little more specific than "bacterial have figured this out"? Are you suggesting that they have very recently evolved to do this after the application of anhydrous ammonia became common, or is there enough naturally occurring anhydrous ammonia in the environment that this pathway exists already? Can you also re-read the question (the part explicitly labeled Question:) and address it specifically? Thanks!

as soon as the ammonia hits the dirt, it stops being anhydrous. also, bacteria have always known how to do this

OK that's very helpful! Would you consider addressing the question as asked: Question: Is it common for most soil bacteria to make significant quantities of nitrous oxide after ammonia is added, or is there only a small subset of bacteria present in soil that might do this? Also, what is the metabolic pathway in this case? Is this a waste product from "eating" ammonia, or something more complicated/subtle?


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Bird brain-eating Mantis - how does it crack the skull?
The New York Times' Science article Birds Beware: The Praying
Mantis Wants Your Brain is a good read and is well researched. Apparently the larger Mantises have been documented to occasionally kill and eat (parts of) birds on six continents.

The mantis was clinging with its back legs to the rim of the feeder, holding its feathered catch in its powerful, seemingly reverent front legs, and methodically chewing through the hummingbird’s skull to get at the nutritious brain tissue within.
“It was staring at me as it fed,” Mr. Vaughan said. “Of course, I took a picture of it.” Startled by the clicking shutter, the mantis dropped its partially decapitated meal, crawled under the feeder — and began menacing two hummingbirds on the other side.

The article continues:

James V. Remsen of the Museum of Natural Science at Louisiana State University and his colleagues documented 147 cases of mantis-on-bird predation in 13 countries representing all continents but Antarctica — not surprising, Dr. Remsen said in an interview, since there are no mantises on Antarctica.
Hummingbirds were the most common target, but mantises also went after warblers, sunbirds, honeyeaters, flycatchers, vireos and European robins. Large species like the Chinese mantis, which grows to four inches in length, were the most avid avivores, and females were responsible for virtually all the bird-killing observed worldwide.
In two reported cases, females feasted on birds while copulating with males. Sometimes the mantises would tuck in through the bird’s breastbone, but more often they went for the head, Dr. Remsen said.
“They bite in and eat the brains,” he said, “which might imply this is something they’re professionals at.” (emphasis added)

Question: How does the mantis break through the skull? I'm guessing it is smooth and much larger than the insects mouthparts, so it can't crush it. Does it cut through somehow? Or maybe go in through the ear? (Yuck!) What "tools" does the mantis have at its disposal to break through a bird's skull?
note: The link is to Bird Predation By Praying Mantises: A Global Perspective, Martin Nyffeler, Michael R. Maxwell, and J. V. Remsen, Jr., The Wilson Journal of Ornithology 129(2):331-344. 2017, https://doi.org/10.1676/16-100.1

below: "An unlucky hummingbird caught by a mantis at a feeder in Colorado." From here. Credit Tom Vaughan/FeVa Fotos


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What exactly does the phrase "chimerical sharing" mean in this abstract?
The Gizmodo article Australian Siblings Are Semi-Identical Twins, Some of the Rarest Humans Ever links to the new paper in NEJM Molecular Support for Heterogonesis Resulting in Sesquizygotic Twinning Gabbett et al. N Engl J Med 2019; 380:842-849 DOI: 10.1056/NEJMoa1701313.
The abstract of this paper says:

Sesquizygotic multiple pregnancy is an exceptional intermediate between monozygotic and dizygotic twinning. We report a monochorionic twin pregnancy with fetal sex discordance. Genotyping of amniotic fluid from each sac showed that the twins were maternally identical but chimerically shared 78% of their paternal genome, which makes them genetically in between monozygotic and dizygotic; they are sesquizygotic. We observed no evidence of sesquizygosis in 968 dizygotic twin pairs whom we screened by means of pangenome single-nucleotide polymorphism genotyping. Data from published repositories also show that sesquizygosis is a rare event. Detailed genotyping implicates chimerism arising at the juncture of zygotic division, termed heterogonesis, as the likely initial step in the causation of sesquizygosis.

There are several terms I am trying to understand here:

sesquizygosis and sesquizygosity: A postulated form of twinship, in which individuals share between 50 and 100% of genetic identity by state (number of shared alleles).
heterogonesis: The assortment of two or more paternal genomes into distinct cell lineages after polyspermic fertilization of an ovum.
juncture of zygotic division (?)
chimerism

So far I understand that the chimerism means for each fetus, some cells have a distinct genome from other cells, and sesquizygosity means (at least) that there is DNA present from more than one sperm.
But I don't understand what "...chimerically shared 78% of their paternal genome..." means exactly when speaking about twins. What does chimerical sharing mean in this case? Are we talking about four genomes (two genomes in each of two fetuses)? If so, how does that comparison reduce to a single value of 78%?

Heterogonesis \ he-tə-rō-gō-ˈnē-səs \
The assortment of two or more paternal genomes into distinct cell lineages after polyspermic fertilization of an ovum.

Visual Representation:

This term — chimerical sharing seems to be used only in this study as a google search did not return any other results. So, it is not a standard term. I believe what they mean by this term is that the twins shared x% of the paternal genome but the sharing is not homogeneous for each cell. In other words each twin has some cells with genetic material from sperm-1 and the others with genetic material from sperm-2.
If the two sperms were genetically identical, then you would not see any chimerism. Let's now consider only one allele as a marker of paternal parentage. So, there will be two populations of cells for each allele.  If both populations are of the same size then you would have 50% chimerism in a single individual (i.e. the allele frequency). The percentage of chimerism may be different between the twins.
Now, there may be several genomic regions at which the paternal-genomes differ. Since the paternal chromosomes would not be symmetrically partitioned between the blastomeres, the different genetic markers (alleles) are likely to have different extents of chimerism.
In this study they measured the frequencies of a few SNPs that were informative for deducing the parentage.

Analysis of SNPs from twin amniotic fluid and parental blood showed
  that 265,489 maternal and 179,205 paternal SNPs were informative for
  parent of origin.

They noted that ~78% of the paternal SNPs were found in both the twins.

Of these, the twins shared 265,400 maternal and 139,155 paternal SNPs,
  which makes them 100% maternally identical and 77.7% paternally
  identical.

Note that this is just a qualitative test for the presence or absence of the alleles. This does not say anything about the extent of chimerism of different alleles. (There are some figures in the supplementary data for the frequencies of different SNP but they are not in a tabular form and hence difficult to deduce).

I appreciate the help, the edit has thrown me off a bit. When I read "...if both types of cells are in equal numbers then you would have 50% chimerism in a single individual." should I understand "50% chimerism" to refer to fraction of cell types, fraction of cell numbers, or fraction of genome that is chimeric?

@uhoh In that case I meant the fraction of cellular genotypes in the individual.


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Any simulations of four-winged dinosaur flight? (microraptors)
This week's podcast of the BBC's Science in Action includes a section by Rory Galloway (12:20 to 18:30) covering the Dinosaurs of China exhibit currently hosted by Wollaton Hal at the University of Nottingham, and includes an interview with curator Dr. Adam Smith.
The exhibit is of highly detailed dinosaur fossils from Liaoning, China where detailed feather structures were well preserved and have been analyzed in great detail.
One section caught my attention:

Rory Galloway: "The similarity between dinosaurs and birds was far more than superficial though. Eventually a branch of small, theropod dynosaurs evolved into the birds that fly around today. But curator Adam Smith says, if we concentrate on flight alone, it gets quite difficult to know exactly which branch of the dinosaurs actually became our birds."
Adam Smith: "Flight is really important and that’s why it evolves many times. Some of the earliest flying dinosaurs, such as the microraptor actually had four wings, not two."

The Wikipedia article on the Microraptor is quite long and includes a lengthy, technical discussion on just how these four wings might have been used. It seems that it is (currently) generally believed that these dinosaurs had the capability of powered flight, and that they could actually take off from the ground, rather than climb trees, jump, and simply glide.
This is with four wings.
There are many variety of insects with four wings and the two pair are used in a variety of different ways. But these dinosaurs are much larger, of the order of a kilogram.
Question: Have there been any complete simulations of the mechanics of four-winged dinosaur flight, showing how the wings would have been used to take off from the ground and gain altitude? A movie or animation of the coordinated flapping of the front versus rear pair of wings would be great. These days the numerical models and computing power are within reach, but it would still be a substantial effort, so I'm not sure if this has been done yet or not.
I'm assuming that this is not currently believed to be the branch of dinosaur that eventually evolved into modern birds, but it's a fascinating branch nonetheless.
below: from here.

@GerardoFurtado then avert your eyes and relax! In biology, the word "similarity" does not have a precise definition as it does in mathematics. It's perfectly fine to address the similarities and differences between any two things. If you have not listened to the entire segment, 12:20 to 18:30, I'd invite you to do so now, and put the quote back into context as any scientist would. :)

@Gerardo Furtado: No, it's the same as "the similarity between mammals and reptiles".

@user24284 The author was clearly using the term dinosaur in the popular sense of 'non-avian dinosaurs', not the clade Dinosauria.

Related: https://biology.stackexchange.com/questions/17546/were-there-any-flying-dinosaurs

Note nowhere in the article does it mention the rear wings flapping. The rear wings do not provide lift, they are acting as control surfaces to improve stability and maneuverability. (think of the tail of a plane).earlier/proto flies have far more demand for control surfaces than developed/derived fliers due to lacking more precise control of flight surfaces.
They basically take off just like any other bird, if they could fly. Flight in dinosaurs likely did not even evolve from gliding as we commonly think of it but instead from raptorian pouncing, the sprawled posture of microraptor you sometimes see, with its hind legs spread wide, is anatomically impossible, you literally have to dislocate both legs to do it. Dinosaur hip joints do not allow for much lateral extension unlike mammalian or varanid ones, more like a hinge than a ball and socket.
The animal in flight would have looked like this.

Hall, Justin, et al. "A new model for hindwing function in the four-winged theropod dinosaur Microraptor gui." JOURNAL OF VERTEBRATE PALEONTOLOGY. Vol. 32. 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA: TAYLOR & FRANCIS INC, 2012.

Thank you for setting me straight on the flapping! Searching on the title of Hall et al. immediately gives oodles of open access further reading; ((almost) all pdfs) 1, 2, 3, 4, 5, 6...

The actual original source was part of a conference so all that was physically published was an abstract as part of the conference issue of JVP. This quirk pops up occasionally in paleontology because there are not that many of us and the Society of Vertebrate Paleontology yearly conference is big enough to cover a significant portion of us. So the feeling is if you are interested you will go. There has been talk for years of recording putting the full talks up online but the cost has been a major delay. Like always the media likes the strangers less accurate interpretation.

There is a good attempt at a simulation of 4 winged flight of Microraptor on BBC's Planet Dinosaur.
There's another  Planet Dinosaur video about their venomous teeth and hunting tactics.
And a Microraptor locomotion video on Attenborough's Conquest of the Skies (Sky 3D).

new dinosaur question: Would anything limit an “invasive species” T. rex introduction now besides running out of food or intervention by humans?

Several models have been proposed, challenged, and revised over the past two decades:

Origin of Flight: Could ‘four-winged’ dinosaurs fly?, Nature (2005)

A previously published reconstruction shows that the hindwing of Microraptor supported by a laterally extended leg would have formed a second pair of wings in tetrapteryx fashion. However, this wing design conflicts with known theropod limb joints that entail a parasagittal posture of the hindlimb. Here, we offer an alternative planform of the hindwing of Microraptor that is concordant with its feather orientation for producing lift and normal theropod hindlimb posture. In this reconstruction, the wings of Microraptor could have resembled a staggered biplane configuration during flight, where the forewing formed the dorsal wing and the metatarsal wing formed the ventral one.

Biplane wing planform and flight performance of the feathered dinosaur Microraptor gui, PNAS (2007)

Model tests of gliding with different hindwing configurations in the four-winged dromaeosaurid Microraptor gui, PNAS (2009)
Paleobiology and the origins of avian flight, PNAS (2010)
Distorted Microraptor specimen is not ideal for understanding the origin of avian flight, PNAS (2010)
Additional specimen of Microraptor provides unique evidence of dinosaurs preying on birds, PNAS (2011)
Aerodynamics of the tail in Microraptor and the evolution of theropod flight control (2012)
Aerodynamic performance of the feathered dinosaur Microraptor and the evolution of feathered flight, Nature Communications (2013)
Shifts in stability and control effectiveness during evolution of Paraves support aerial maneuvering hypotheses for flight origins (2014)
Aerodynamic Characteristics of a Feathered Dinosaur Measured Using Physical Models. Effects of Form on Static Stability and Control Effectiveness, PLOS (2014)
The aerodynamics of gliding flight and its application to the arboreal flight of the Chinese feathered dinosaur Microraptor, Biological Journal of the Linnean Society (2014)
HINDWING FUNCTION IN FOUR-WINGED FEATHERED DINOSAURS

new dinosaur question: Would anything limit an “invasive species” T. rex introduction now besides running out of food or intervention by humans?


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Why did they expect Astronaut Scott Kelley's telomere shortening to accelerate? (they got longer!)
The NPR News article and podcast Scientists Share Results From NASA's Twins Study says:

SCOTT KELLY (NASA Astronaut): You know, the symptomatic stuff is fine. I don't have any long-term negative feelings, physically, from being in space. Now, there's the things you can't feel. And hopefully, I will never learn that those are a problem.
GREENE (Host): Those things you can't feel - well, it turns out they are as small as the protective structures at the ends of his chromosomes.
MARTIN (Host): Yeah. These are called telomeres, and normally, they get shorter with age. But what about in space?
SUSAN BAILEY (Principle Investigator): What we wanted to do was evaluate telomere length in both of the twins before and after so that we could see, you know, where they started and then where they ended.
MARTIN: Susan Bailey was one of the scientists who answered this question. She expected the stresses of space to shorten telomeres quicker.
BAILEY: And, in fact, we saw exactly the opposite thing - that during spaceflight, he had many more long telomeres than he did before he went up. So that really couldn't have been more of a surprise to us.

See also Radiation Biologist Dr. Susan Bailey Studies the Cellular Clocks of Astronaut Twins
Question: Why did investigators initially believe that Scott Kelley's year in space would accelerate the rate of telomere loss, relative to his baseline rate and the rate of his identical twin brother on the ground? What would be the postulated mechanisms?

I've added the radiation tag since it is a known difference between spending a year in space versus on the ground, but I don't know if that will be part of the answer  or not.

Dr. Bailey wrote a short piece that hints at the reasons behind why she expected what she expected:

Telomeres are the ends of chromosomes that protect them from damage and from “fraying” – much like the end of a shoestring. Telomeres are critical for maintaining chromosome and genome stability. However, telomeres naturally shorten as our cells divide, and so also as we age. The rate at which telomeres shorten over time is influenced by many factors, including oxidative stress and inflammation, nutrition, physical activity, psychological stresses and environmental exposures like air pollution, UV rays and ionizing radiation. Thus, telomere length reflects an individual’s genetics, experiences and exposures, and so are informative indicators of general health and aging...
Our study proposed that the unique stresses and out-of-this-world exposures the astronauts experience during spaceflight – things like isolation, microgravity, high carbon dioxide levels and galactic cosmic rays – would accelerate telomere shortening and aging. To test this, we evaluated telomere length in blood samples received from both twins before, during and after the one year mission.


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Taxonomy and 'breeds' of animal species
How do taxonomists classify breeds of organisms in a species? When talking in such depths about organisms (using RNA and DNA), don't they have to unavoidably do it?
I read in another question that all the breeds of dog we domesticate belong to the same species. But they (the dogs) certainly have very apparent differences. Don't they?
So how do taxonomists handle/consider these 'breeds'?

Take at look at this.


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What is the metagenome like for other classes of animals?
Lately there's been a lot of discussion around the many non-human cells essential to a healthy human body — called the microbiome, or metagenome.  Much of this is in the gut microbiome.  See this question, for example.
The Human Microbiome Project at NIH emphasizes we are just beginning to measure the specifics of this for the human case.
I assume this is similarly true for all mammal species, and I don't know how much farther.  Fish have a fairly different body plan than mammals, including a fairly different gut. And coelenterates have an even more different body plan in many ways, again including the gut.
Does a typical fish depend on as large a microbiome as a human?  Is there much known about that?  What about jellyfish?

There are multiple parts to an answer for this.
1) There is not only a microbiome in the gut. So microbiomes in general are very diverse. A fish microbiome on the scales will of course be very different to the one on a human skin.
2) Gut microbiomes are also quite different both in taxonomic and functional content, as they are in different ecological niches.
3) There are microbiome studies for nearly every type of organism I could imagine now. Fish, insects, snakes, you name it. They differ in diversity and composition of their microbiome, but also the used methods and databases do differ, so it is hard to compare them.
4) The further away from well studied microbiomes we get, the less specific will be our assignment of taxonomy and function, because we have not seen enough comparable microbes before. So more information will be hidden in the "dark matter" (in metagenomics: reads not assigned to a taxon and/or function).
Unfortunately I don't know of any jellyfish microbiomes so far. Their body (as far as I know ) seems to be much more "permeable" for sea water (-> their environment) and thus I would think that they generally would have aquatic bacteria in whatever corresponds to their gut. The sea microbiome is said to be very diverse and far too little studied, although there are cool projects like the Global Ocean Sampling Day to try and close this huge gap as best as possible.

Fish scales are an interesting example to think about.  It seems pretty likely that some of the microbiota on the scales are clearly essential to healthy function (once you understand what they are really doing), and others not at all important for good or ill. It could be a hard problem to figure out the difference between metagenome and plain old parasitism or mere proximity.

@ColinMcLarty I think you are misinterpreting the term metagenome. It does not exclude parasites or only include species essential to health. If it lives in your X (gut, mouth, urinary tract, skin ...) it's part of your X metagenome.

@CharlesE.Grant Ah.  In fact looking at https://en.wikipedia.org/wiki/Metagenomics I see it was not originally an organism that had a metagenome at all, but an environment--say a dirt sample, a stream, or a human gut.  That article suggests many people still use the term that way.  But NIH has their project on "the human metagenome."

@ColinMcLarty, Its the same usage. It's just considering an entire organism (humans) as the environment.


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Using Chi-squared analysis to confirm expected phenotypic ratios of offspring
In a recent question the original poster was faced with deciding which ratios to use in a Chi-squared analysis. They were supposed to decide on, "logically", what test-ratio to use.
Example question:
A supplied sample contains four types of seeds and the total number is 64. The
types of seeds are large red 42, large white 8, small red 10 and small white 4. Calculate goodness of fit.
My initial assumption was that in order to solve the problem, you would need to think about the genotype of each parent.
Lets say:
L = large seeds;
s = small seeds;
R = red seeds;
w = white seeds
If both parents were LsRw, the phenotype-distribution of the offspring would follow a 9:3:3:1 ratio.
If one parent was LsRw, and one parent was ssww, you would have a 1:1:1:1 ratio.
And if one parent was LsRw, and the other parent was Lsww or ssRw, you would have a 2:2:1:1 ratio.
Obviously, out of all of these ratios, the example question follows most closely with the 9:3:3:1 ratio.
So, to solve this question statistically, would you make the null hypothesis There is no difference between the observed and expected ratios?
While the alternative hypothesis would be There is a different between the observation and the expected ratios?
And would a statistically significant result indicate that the null hypothesis must be rejected in favour of the alternative hypothesis, thus the parents are unlikely to be heterozygotic for both traits?

I suspect that the actual question contained more information than what was posted. If not, presumably you could formulate a null and alternate hypothesis for each expected ratio to determine the phenotypes of the parents, though as I type this I can't help but think there would be some statistical reason not to do it this way. Perhaps you would get a better answer at Cross Validated.

You're correct, each time you run a statistical model you are introducing an error of ~5% to your conclusion - that would be the reason to not do it that way. But this question has had me thinking for a couple days so I thought I'd see if anyone has any other approaches to the problem with the limited information available. If indeed it is a matter of just thinking about inheritance, I'm not sure if the statisticians would be able to catch on.

For any statistical test the definition of the null hypothesis is essential. You cannot guess the null hypothesis based on a given question. The null hypothesis is based on some prior knowledge. There is no way to guess it. Moreover, what the alternative hypothesis is does not really matter because the statistical test does not say which one of the infinite possible alternatives is correct. The test just accepts or rejects the null hypothesis and for any test the first step is to define the null hypothesis; everything else is after that. Plus, a test cannot be performed with just one sample!

In the example you considered, the null hypothesis is basically that observed value is not different from an expected value for which the prerequisite is the knowledge of the expected value. Now what the expected value is, depends on your model. You assumed one possible inheritance model and proceeded towards calculation. However, this assumption has to be clearly stated and understood by the experimenter before performing the test. OP's professor did not talk about any underlying model and simply asked to check goodness of fit. It is ridiculous; I can assume anything as per my convenience.


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What cells in mosses behave analogously to mammalian embryonic stem cells?
The Washington Post article Ancient life awakens amid thawing ice caps and permafrost describes the work of Peter Convey, an ecologist with the British Antarctic Survey and his team, and includes a discussion of some mosses that have survived over 1000 years in permafrost, and sprung to life once "revived" in a laboratory setting.
This passage caught my eye:

It’s not easy to survive being frozen solid. Jagged ice crystals can shred cell membranes and other vital biological machinery. Many plants and animals simply succumb to the cold at winter’s onset, willing their seeds or eggs to spawn a new generation come spring.
Mosses have forged a tougher path. They desiccate when temperatures plummet, sidestepping the potential hazard of ice forming in their tissues. And if parts of the plant do sustain damage, certain cells can divide and differentiate into all the various tissue types that comprise a complete moss, similar to stem cells in human embryos.

What are these cells in moss called, and how similar are their functions to mammalian embryonic stem cells?

Convey and his team announced that they had awakened 1,500-year-old moss that had been buried more than three feet underground in the Antarctic permafrost. (P. Boelen/BAS)

The growing tips of roots and shoots contain regions of rapidly dividing cells in all plants that are called apical meristems. Apical meristems contain the plant's stem cells, which are not fundamentally different from the stem cells of animals.
You can begin learning more about this subject from this Nature scitable article.

This is just what I needed... reading now, thanks!

Great! Glad I could help.

Cambium also has totipotent stem cells as you might know that some plants can be propagated by planting stem cuttings.

@WYSIWYG — True and also from callus, but unless I'm misremembering only vascular plants have a cambium and so that didn't seem relevant to bring up in a post about mosses.


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Was 14,000+ year old DNA "laying around in cave dirt" protected from degradation, or is it just naturally this robust?
In the NYTimes news article No Bones About It: Scientists Recover Ancient DNA From Cave Dirt I've read:

Although DNA sticks to minerals and decayed plants in soil, scientists did not know whether it would ever be possible to fish out gene fragments that were tens of thousands of years old and buried deep among other genetic debris.

I haven't read the original article yet, but I'd like to double check, this is bare DNA molecules, stuck to minerals or other detritus in 14,000 to 550,000 year old compacted dirt? Roughly speaking at least? In layman's terms, just laying around in some caves?
Has something protected the DNA from degradation, or is DNA just more environmentally stable and robust than I thought?
There is also discussion in the Science commentary No bones? No problem: DNA left in cave soils can reveal ancient human occupants.
The NYTimes article goes on to say:

The new study involved searching for ancient DNA in four caves in Eurasia where humans were known to have lived between 14,000 and 550,000 years ago.
Dr. Meyer and his colleagues figured out which DNA in the cave sediment was prehistoric by looking for telltale signs of degradation at the ends of the molecules.

What are the "telltale signs of degradation at the ends" of DNA molecules described in the paper?

need help choosing proper tags...

To be clear they are not finding long DNA strands but short fragments. DNA becomes more robust the shorter it gets. Fragments can last millions of years. The local chemical conditions have a huge influence on how long DNA lasts the oldest being hundreds of millions of years old under ideal conditions.
The ones the archeologists are finding are not even close to enough to rebuild an intact strand but it can be used for matching. Of course contamination is a big problem, anything that dies leaves DNA in the soil. With humans it becomes especially problematic becasue the archaeologists themselves are a major source of contamination.
For an indepth look at contamination protocols, some of which as still questionable, can be found here. Sorry its behind a pay wall.
Likely they are referring to deamination cytosine substitution, which creates mismatched pairs of DNA and occurs more and more as DNA ages.

OK I'll get a hold of the paper soon. When you say millions of years, is that necessarily when found in marrow enclosed in an unbroken bone? Does deamination cytosine substitution refer to the type of process described here: https://en.wikipedia.org/wiki/Deamination#Cytosine ?

"Fragments can last millions of years": citation needed. I'm not saying you're wrong, I just find that surprising (though I am no biochemist so that doesn't mean anything) and would like to read a reference backing it up.

http://www.sciencedirect.com/science/article/pii/0016703794901856  As they mention DNAhas been recovered from amber preserved insects many times. amber vastly retards DNA decay that's why finding a Dinosaur tail preserved amber is so exciting! In the end DNA decay is not like radiometric decay with a largely unaffected rate, local chemical conditions have a huge influence.

@uhoh not necessarily, although depending on the local chemical conditions it may be possible. DNA decay in heavily influenced by local chemistry it's not like nuclear half lives.

OK this is great - Thank you for adding Amino acid racemization in amber-entombed insects... This will make great reading!


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Is the "Manhattan Ant" a new species; still only found in Manhattan's Upper West Side?
I've stumbled upon the viewing.nyc article Upper West Side Has Its Own Ant Species Dubbed the "ManhattAnt" which says:

Columbia University biologist Rob Dunn has discovered a unique species of ant living between 63rd and 76th streets along Broadway on the Upper West Side of Manhattan. Dubbed the "ManhattAnt", the ants have a higher concentration of carbon in their bodies, indicative of a high corn-syrup diet, likely from eating trash and discarded street food.

Biologists stumbled upon a new species of ant in the Broadway medians at 63rd and 76th streets […] The ant looks like it hails from Europe, but so far the scientists have not been able to match it with any of the approximately 13,000 species of known ant. “It’s new to North America, and we believe it’s new to the entire world,” biologist Rob Dunn, whose team discovered the insect, told the Post. The ant doesn’t have a scientific name yet, but it’s fondly nicknamed the “ManhattAnt.”

and references the Simthsonian Magazine article NYC Has Its Own Ant, the “ManhattAnt” with the subtitle:

A new ant species joins a menagerie of other creatures cut off from their kind in isolated patches of urban green in NYC

A "new species" is not the same thing as a "creatures cut off from their kind in isolated patches of urban green in NYC"
Question: Has the "Manhattan Ant" or "ManhattAnt" turned out to be a new species, and is it still only found in Manhattan's Upper West Side?

I'm not sure that the species-identification tag fits here. Those who are monitoring the tag and have species-ID skills may still be interested in answering this question, but I don't have independent images or measurements of the ant. Since "Columbia University biologist Rob Dunn" is cited, there should be some reliable information out there somewhere in the literature, but I don't know how/where to find it.

I'm not sure what we can add to this. The article states that for the moment, this does indeed look like a new species. But it was only identified a few months ago, so there's not much more to say. It's not as though this was several years ago so you can expect a consensus to have been reached.

@terdon the site has a substantial number of active users; I wouldn't write each and every one of them off so quickly. Sometimes people actually happen to know specific information on a topic, and this species, having been reported in several news sources, and relating to an interesting new topic in biology (species differentiation affected by urban development), might just have an extra amount of notability in the field. Let's wait and see!

I say this because your question suggests you were under the impression that the species was discovered years ago:  Has the "Manhattan Ant" or "ManhattAnt" turned out to be a new species, and is it still only found in Manhattan's Upper West Side?

@terdon based on the answer below I found essentially the same article published in 2012! https://nypost.com/2012/09/02/new-breed-of-ruffi-ant-found-in-manhattan/

yes indeed! I'm glad you found out more :)

Rob Dunn is a professor at North Carolina State University (though apparently taught at Columbia University at some point). I recall him mentioning this specific NY ant discovery to me 4-5 years ago. A better pop-sci article can be found here that suggests this discovery was circa 2012. Another related article can be found here.
You can find a few other papers regarding urban ant populations by Dunn and collaborator Amy Savage and others via Rob Dunn's website, (Ex: Savage et al. 2014 and Penick et al. 2015).
However, I could not find evidence in the few relevant papers I skimmed for the the so-called "Manhattant" or evidence of any publications formally introducing this as a new species.
Pećarević et al. 2010 ("Biodiversity on Broadway - Enigmatic Diversity of the Societies of Ants (Formicidae) on the Streets of New York City") lists a number of species found by Dunn and others in Manhattan, but again makes no mention of this specific discovery.
My conclusion is that since Dunn has not listed this as one of his many publications on his website it's either burried in another paper as an ancillary artifact, or, more likely, has not been formally described...
You could reach out to Rob directly [email | twitter], I suppose, and update us all on this question!

This is great, thank you! The Biodiversity on Broadway paper (Pećarević et al. 2010, yay, open access!) is quite interesting, and google for example gives 55 citations and many related papers So this will keep me busy for a while. I'm too shy to reach out directly to any of them being outside my field, but that's a good idea and someone may follow up on it.

apparently there is an Ant Wiki for this too! http://www.antwiki.org/wiki/Ants_of_New_York_City


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What do halophytes do with the salt?
The answer to "How do some plants grow in salt water, while others die?" offers some hints as to how salt-tolerant plants store salt by shifting it out of cells, and also can deal with higher salt concentrations in cells, but what happens after that?  Do the plants somehow excrete the salt? Store ever-increasing amounts in more and bigger vacuoles? Convert it into something more useful by chemical reactions? Reach equilibrium concentrations with the water in which they grow and rely on osmosis?
It seems to this layman that plants growing in salt-water in the tropics will transpire quite a lot of water, and if that's replaced with salt water, they'll take up quite a lot of salt.

There are a couple of strategies that salt-tolerant plants can use to survive in high-salt conditions.
Plants can increase the concentration of compatible solutes in their cell to the point where the intracellular concentration of solute approaches the concentration of the water in the environment. By doing this, the plants are able to minimize water loss through osmosis, while ensuring that the cells do not reach harmful levels of salinity.
However, compatible solutes are often not enough to completely combat the effects of salt stress. Salt stress creates higher concentrations of oxygen free radicals, which can cause harm to DNA and other cell components. Mangrove trees have been found to have heightened expression of repair proteins and anti-oxidants when exposed to salt stress.
Additionally, mangroves have been found to be able to excrete salt from their root cells and their leaves. They have ion-transporters which actively pump sodium ions out of their cells into the extracellular space. They have salt-filtering mechanisms that allow them to uptake the water from salt-water without up-taking the salt in the water.
So in conclusion, salt-tolerant plants sequester some salt within their cells, but also use ion-pumps and compatible solutes to limit the concentrations of salt within their cells. They can selectively uptake water from salt water, and use repair mechanisms to limit the damage of high salt concentrations in their cells.
Kao, C.H. 2015. Mechanisms of salt tolerance in rice plants: compatible solutes and aquaporins. Crop, Environment & Bioinformatics 12:73-82.
Wang, L., Pan, D., Lv, X., Cheng, C.L., Li, J. Liang, W., Xing, J, and W. Chen. 2016. A multilevel investigation to discover why Kandelia candel thrives in high salinity. Plant, Cell & Environment 39:2486-2497.
Srikanth, S., Kaihekulani, Lum, Y., and Z. Cheng. 2016. Mangrove root: adaptations and ecological importance. Trees 30:451-465

I'll have to follow the references when I'm back on a network with journal access but already I'm greatly enlightened.


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Seeing through the rain
This question leads me to wonder about seeing in and through rain.
From visual point of view, rain is light-bending droplets moving downwards, unformly in steady rain, less uniformly if there's variable strong wind. At least human brain is pretty good at filtering out the rain and seeing the stationary background.
Is this ability just physics, and no special adaptation needed? Or is it a biological ability, our eyes and brain doing some "heavy lifting" to be able to see as far as possible in rain?
If it is biological, evolved ability, then is there difference between different animals on how well they see in rain, compared to how well they see in clear weather? Has the ability evolved rarely, or does it arise naturally and easily if it gives advantage to a species? I suppose the only interesting animals here are those, which see far in clear weather to begin with.
I'm obviously looking for some real research done on the subject, not just speculation.


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What species of eagle pushes their young to teach them flying?
There are many references to eagle pushing their young off the nest to make them know how to fly, for example this motivational video.
It is also described in this website:

Let me show you "the ways of an eagle" in the nest, and give you a picture of our lives as well. After the eaglets get to a certain size, or maturity, everything changes! One day the mother eagle comes back from being gone, but this time there’s no food in her beak, and she doesn’t land on the edge of the nest. Instead, she hovers over the nest.
You may not know this, but an eagle can do almost what a hummingbird can do. Even though they are great birds, they can remain almost motionless in midair with those great wings just undulating in the breeze. They do this about three feet above the nest. I’m sure if little eagles could talk to one another—and maybe they can—one would certainly say, "My, what strong wings Mommy has."
Why does the mother do this? She is demonstrating that those curious appendages on the babies’ backs have a useful function. Eagles, of course, were meant to fly, but they don’t know that. If we take an eagle and separate it at birth from its parents, it will never learn to fly. It will just grovel around in the dirt like a chicken. It might even look up and see eagles soaring overhead and never guess that it was meant to soar in the heavens.
Eagles have to be taught, and that’s the mother’s job. So first she just demonstrates.
The next thing she does is come down into the nest and surprise her young. One can imagine how warm it must normally be for the little eagles to snuggle with their mother and be enshrouded with her feathers, but this time she puts her head up against one of the little ones, and pushes that little one closer and closer to the edge of the nest. ("Hey mom, mom, what are you doing?")
All at once she pushes the little one out of the nest, and the eaglet falls down the face of the cliff, surely to be destroyed. But not so! In a flash the great mother eagle flies down, catches the little one on her back, and flies up and deposits it in the nest. ("Whew! Mom, that must have been an accident.") But it wasn’t an accident. The mother bird pushes the little one out again, and again, over and over.
Why would a mother do that to her young? Does she hates the little one? Not at all. It’s just that those little birds were made to fly, and they don’t know it, so she is going to push them out of the nest. She never lets them hit bottom, but she does let them fall, because they have to learn something they don’t know.
The next time the mother bird comes back she decides to clean house, and so she stands on the edge of the nest. The first things to go are the feathers inside; she drops them over the edge. Then the leaves go over the edge—heave ho! While this is going on, she’s not very talkative, either. ("Mom, what are you doing?") She pays no attention. Since she built the house, she knows how to take it apart.
Next she decides to take the sticks out of the middle of the nest, and with her great strong beak and feet, she’s able to break them off and stand them straight up. ("Mom, it’s not comfortable in here anymore.") Then she takes certain key sticks out of the nest and throws them over the edge. ("What are you doing, Mom? You are wrecking my room.")
She seemingly pays no attention to the concerns of her young as she prepares to pull the nest apart, for she is determined that those little ones will fly, and she knows something they don’t. She knows they will never fly as long as they remain in the nest.

However, looking at this very interesting documentary on white-tailed eagle, the young eagles don't learn to fly by getting pushed as described in the motivational video, but they learned flying by practicing their wings on good winds.
Looking from the nesting place (cliff), I read that it might be Golden Eagle. But the section describing the fledgling doesn't say anything about the parent eagle pushing the young, although it does say about "jumping off":

The first attempted flight departure can be abrupt, with the young jumping off and using a series of short, stiff wing-beats to glide downward or being blown out of nest while wing-flapping. The initial flight often includes a short flight on unsteady wings followed by an uncontrolled landing.

Does Golden Eagle really push their young to teach them flying? If not, which species is it?
In case it's not clear, I am also interested in references that describes the eagle behavior in more details. It would be good if there is a video documentary, but considering that capturing this moment on tape might be difficult, that's not my utmost concern.

I am pretty sure this doesn't happen with eagles, and I have no idea why this would be written.

But not so! In a flash the great mother eagle flies down, catches the little one on her back, and flies up and deposits it in the nest. ("Whew! Mom, that must have been an accident.") But it wasn’t an accident."

This is flight, alright: a pure flight of fancy.
There have been many hundreds of videocams set up in all kinds of remote locations so that behavior in the wild can be studied. Some of the most popular cams in recent years have been the eagle cams (e.g. at eagles.org). They are live during nesting season and record for all the behavior of eagles.
If the parents did not feed their young, as described in the fabrication above, the young would starve to death, as it takes time to learn to fly. If anything, the eagle parents must increase the feeding to keep up with the nutritional needs of the growing chicks, and the muscle building taking place. The parents don't stop feeding until a while after they're flying well.
Eagles don't learn "learn" why they have wings by observing the mother eagle hovering above them (pure anthropomorphizing). They leave the nest and start roaming on the branches, practicing hopping, landing, and building up their wing strength. Eventually flying, they still come back to the nest to feed. In this video from British Columbia (not the most exciting in the world) you can see exactly this happening with bald eagles. Eventually the young eagles scavenge and learn to hunt for themselves. It takes time. This page describes the fledgling feeding and flight behavior.
While I am not going to try to find an eagle that behaves in the bizarre manner you've found and asked about, I will say that eagles are eagles and more or less behave pretty similarly. The most common eagle in the world is the bald eagle. The Golden behaves like the Bald. Eagle behavior is influenced by habitat, etc. Wikipedia has a page listing 60 species of eagles. Picking a random eagle from another part of the world (in this case, the Sub-Saharan Martial eagle, this information seems to confirm that attentiveness of adult eagles and fledgling behavior is similar though not without species variation:

Martial eagles have a slow breeding rate, laying usually one egg (rarely two) every two years. The egg is incubated for 45 to 53 days and the chick fledged at 96 to 104 days. Despite increasing signs of independence (such as flight and beginning to practice hunting), juvenile birds will remain in the care of their parents for a further 6 to 12 months. Due to this long dependence period, these eagles can usually only mate in alternate years.

I'm sure I'm not the first to warn you not to believe everything you read on the internet.

I see. I like the knowledge about eagles that you share, but I sense a slight negativity in the sentiment. Perhaps we can try to discuss in more neutral manner. =)
Btw, can you point out the section in the story above where it describes "the parents did not feed their young"? As shown in the documentary I linked in my question (starts from 20:20), the parent eagle did still feed the young, but it also did limit the food given to the young, to encourage the young to find food themselves.

"One day the mother eagle comes back from being gone, but this time there’s no food in her beak, and she doesn’t land on the edge of the nest. Instead, she hovers over the nest." Yes, there is negativity. A lot of that passage is pure fabrication, which I do not like, and feel is an ethical violation, hence the sentiment you correctly picked up on. There is no reason at all to take a kindly attitude towards the spreading of falsehoods.

Can you confirm what I noticed in the documentary? I copy again here: "As shown in the documentary I linked in my question (starts from 20:20), the parent eagle did still feed the young, but it also did limit the food given to the young, to encourage the young to find food themselves." This is an observed behaviour, right?