text:
Can humans perceive sounds above 20 kHz?
In the never-ending debate raging in the audiophile community about sound quality and what humans can or cannot hear, it is very very very very incredibly often cited that the upper-limit of the audible range of human hearing is 20 kHz, give or take. Some indicate that this is a conservative estimate, and that the actual upper-limit is actually lower than that (~18 kHz). While others suggest that sounds could be heard or otherwise perceived up to about 25 kHz-30 kHz:

Sampling rates higher than about 50 kHz to 60 kHz cannot supply more usable information for human listeners.

And some others suggest that there is substantial variation between individuals around the upper limit:

The human range is commonly given as 20 to 20,000 Hz, though there is considerable variation between individuals, especially at high frequencies

So is there any biological evidence whatsoever that young, healthy humans can hear or otherwise perceive (or sense) sound waves above 20 kHz? And what would be a conservative estimate of the absolute upper limit of the audible spectrum for humans (i.e. usable sound information for human ears and senses)?

Yes. I personally used to top out at 22-23khz.

@Joshua I'm curious: how was this measured?

Digital frequency generator at constant volume. Kept on increasing frequency until I couldn't hear it. Generator was rated for 32khz.

The last time I had it working I was about 16. That hardware is broken and the replacement couldn't go high enough to repeat the test.

@Joshua Interesting. Being 16 at the time (young teenager, NOT an adult) may explain why you were in the whereabouts of 22 kHz. Here's an online High Frequency Range Test (8-22 kHz).

More concrete answer: Inaudible high-frequency sounds affect brain activity: hypersonic effect (https://pubmed.ncbi.nlm.nih.gov/10848570/)

Yes, we can. By means of bone conduction we can hear up to 50 kHz, and values up to 150 kHz have been reported in the young (Pumphrey, 1950). However, it is indeed generally agreed that 20 kHz is the upper acoustical hearing limit through air conduction. The reason for this is debated, but the transfer function of the ossicle chain in the middle ear is a suspected culprit in setting the upper frequency limit to 20 kHz (Hemila et al., 1995).
Hence, using normal speakers or headphones 20 kHz is a very reasonable absolute upper limit. Note that the Nyquist criterium necessitates higher sampling rates (at least 40 kHz), so your statement of using 50k-60k sound cards is correct. If you decide on using bone conduction aids, you might start to think on using higher sampling rates still.
Here is an example of a commercially available bone conduction head set (AfterShockz):

These devices have the potential to increase the upper limit because they bypass the middle ear and hence circumvent the limiting transfer function of the middle ear. They induce vibrations onto the temporal bone, that travel via the bone directly to the inner ear. See the following picture from The High Tech Society:

As a side note: when you grow older the hearing sensitivities at high frequencies  are severely reduced, and even the 6 kHz range is severely affected in the elderly (picture from John Perr's website):

Disclaimer: I haven't looked into the capabilities in terms of upper frequency limits of bone conduction head sets. I am just talking theoretical limits.
References
- Pumphrey, Nature 1950; 166:571
- Hemila et al., Hear Res 1995; 85:31-44

Thanks! I'm curious what you mean by this: "the maximal acoustic frequencies are quite dramatically undersampled at 50 kHz". This source is making a solid argument that technically the analog sound wave is perfectly recreated up to half the sampling rate (as per Nyquist theory). So if you sample at 96kHz (commonly done), you can recreate perfectly up to 48kHz. Do you mean that some things like harmonics may be missed?

Yeah, I see your point, and that's what I was thinking, too. But that guy seems to be making a serious argument. According to my understanding of his arguments, whether you use 44.1khz or 192khz, the data is always sufficient to perfectly recreate the exact original sinewave (up to the bandwidth limit, here ~22kHz), as per the theory. In each case, there in only one band-limited signal that passes through each sample point, and it is a unique solution (see minutes 5-8 of the video).

One other bit... Do I understand correctly that the reported "substantial variation between individuals" implies that very often adults will have an effective upper limit lower that the generally agreed upon 20 kHz?

Correct. 16 KHz sensitivity for example  dwindles in young adults

Note that the Nyquist sampling limit is the minimum sampling rate necessary to have any hope of reproducing the input signal before the signal becomes unreproducible. At 2f the reproduced signal is potentially distorted. This works well if you don't care about amplitude distortions but only care about the relative phases of the signal (such as for digital square wave signal) but is very poor at accurately capturing full analog signals. For applications other than audio (such as networking, imaging etc) the rule of thumb is to use 1.5 or 2 times Nyquist frequency. In other words f3 or f*4.

Doesn't hurt to note that Shannon-Nyquist assumes you start with a time-based function f(x), NOT a live audio stream. It assumes the creation of stream-accurate samples has already occurred, and concerns encoding them in a reproducible manner. This is not equivalent to the sampling rate required for recording, which can be as high as 10x the maximum desired frequency. For illustration, consider 2 22khz tones immediately next to each other in a 44khz sampling window; the window will express a single 22khz tone, losing the second one. S-N is almost universally mis-applied in this manner.

I think your first sentence misrepresents Pumphrey. He said "As the frequency was varied continuously from 12 to 100 kc./s., the pitch rose with it to 15 kc./s. and stayed there as the frequency was further increased." In other words, he found evidence that high-frequency oscillations could be heard through aliasing at lower frequencies, not that sampling rates above 44.1 kHz are needed to reproduce perceived sounds accurately, even when using bone conduction.

If all the processes through which a signal passes are linear, then it makes sense to speak in terms of a maximum useful-content frequency. If a signal passes through non-linear stages, however, it is possible that frequency content which would in and of itself be above the range of hearing, may interact with other frequency content which is also above that range, in such a fashion as produce artifacts which are well within the range of hearing.
A rather annoying example of that may be observed when a GSM cell phone is located near audio equipment. All of the frequency content transmitted by the phone exceeds the upper limit of human hearing by multiple orders of magnitude, and yet the annoying buzz picked up by the audio equipment clearly does not.
What happens is that the frequency content of the cell phone's transmissions contains numerous frequencies which are separated by tens or hundreds of hertz, and many amplifier stages don't completely filter out the radio-frequency content, but are unable to process it without distortion. This distortion causes the amplifier to output sum and difference frequencies, some of which are very much in audible range.
Many kinds of objects and materials will reflect sound waves in a fashion which varies in non-linear fashion with the sounds being reflected. If a diaphragm which had more freedom of movement in one direction than the other were hit with a mixture of 100,000 Hz and 100,100 Hz tones, it would "buzz" at 100 Hz, whereas it would not do so if hit by either tone alone; further, a conventional recording of the combined tones by a high-quality microphone would detect nothing, so playing it back in the presence of the diaphragm would yield no buzz.
It would be rare for aesthetically-pleasing audio content to have frequency content over 20 kHz which contributed materially to its aesthetic aspects.  It would certainly be possible, however, to construct frequency content over 20 kHz, however, which could be heard in many common environments, and whose perceived sound would vary in ways that would not be possible using only frequencies below 20 kHz, and would not be implausible that some kinds of musical instruments (e.g. handbells) might produce mixtures of high frequency content which would sound different to different people who found them pleasing, in ways which could not be mimicked using only directly-audible frequencies.
It may be possible for an audio technician working with a functional MRI team to create, for an individual, a sound which was indistinguishable from the original, but for another individual that recreated sound might sound nothing like the original.

Very interesting... But how would that work in the context of audio recording and playback? Say a handbell produced a mixture of high frequency content which would have somehow made it's way into the audible spectrum, what would the recording pick up? The ultrasound, or its impact on the audible spectrum? And upon playback, what would make the listener tickle: hearing the recorded audible spectrum, or the ultrasound which would dynamically interfere with the audible spectrum? So, to ensure that the peculiar handbell sounds aren't lost, is it imperative to reproduce the high-freq content?

@landroni: I have neither the tools nor expertise to identify the extent to which frequency aliasing caused by intermodulation of ultrasonic-frequency content affects perception in non-contrived cases.  I would expect that the eardrum would introduce some distortion because of its asymmetrical loading, and that the details vary between one person and the next, but I don't know the extent of the effect or its variation.  I do know that the auditory experience of hearing a handbell concert is different from that of hearing a recording, but I have no idea whether the difference...

...stems from 20Khz content, 30Khz content, 40Khz content, or something else entirely.  A recording at a 44KHz sample rate must not capture anything above 22KHz, though if room acoustics or the microphone caused a combination of higher-frequency sounds to produce a lower-frequency sound, the recording would capture that lower frequency.  My main point is that it's entirely plausible that capturing higher frequency content may, in at least some cases, make a recording sound better even if the content itself would not be directly perceptible.

So am I getting this right: imagine that a handbell concert was recorded at 192 kHz sampling. Then when played back at 192 kHz (without any downsampling), it would be possible that the higher frequency content in the 20-96 kHz band could combine in such away as to produce a lower-frequency sound which would then be audible by the listener... Correct? And in that case, would the playback feature that lower-freq content twice: once from the recording, and once from the playback containing the high-freq sounds which would once more combine to create low-freq waves? I'm slightly confused here...

Or is it instead the case that when the hi-freq content (20-96 kHz) combine in the live performance and the 192 kHz recording equipment captures that lower frequency sound (0-20kHz), and if you downsampled the recording from 192 kHz to 44.1 kHz and played it back, that even then the low-freq content (caused by the hi-freq combination) would still be audible to the listener? In that case the 192 kHz high-resolution recording would be redundant for playback purposes to humans, and safely discarded while keeping just the 44.1 kHz downsampled version...

I guess the ultimate purpose of my question is to determine whether playback of 192 kHz recordings is utterly unnecessary, as all content that we may hear (below more or less 20 kHz) is already within the 44.1 kHz samples (including low-freq sounds generated by high-freq waves)... And whether all recorded info above 44.1 kHz sampling is simply irrelevant for playback purposes...

I suspect the most important kind of intermodulation distortion from the standpoint of human perception would occur within the ears of each individual listener.  One listener might perceive a combination of equal-strength 60kHz and 55kHz as a 5kHz tone whose strength is 20dB down; another person might perceive the combination as a 5kHz tone whose strength is 25dB down.  For the first listener, a recording where the higher frequencies were replaced with a 5kHz tone that was attenuated 20dB would be indistinguishable from the original, but the second listener might find...

...such a recording to be a tiny bit more shrill than the original (for him a proper recording would have attenuated by 25dB).  I would expect the differences to generally be subtle in any case.

...but either way, if recorded at 192 kHz sampling, both the 60kHz and 55kHz waves would not recreate the 5kHz tone when played back, correct? From what I understand, the 5kHz tone would be a product of both high-frequencies and the acoustics of the venue, and would already be recorded within the 44.1 kHz samples... When playing back the recording, humans would only hear what was recorded below 22 kHz, while all those high-freq waves would no longer have the same effect as they did in the venue...

If the listener's ear, when given 60KHz and 55Khz at some amplitude would create a 5KHz signal at a lower amplitude, capturing both frequencies on a 192KHz recording and playing them back would achieve a similar result.  Someone with a good computer model of a particular listener's ear might be able to produce a 44.1KHz recording which that person would find indistinguishable from the higher-quality one, but other people might find the two recordings to be different.

capturing both frequencies on a 192KHz recording and playing them back would achieve a similar result. Very entertaining! Thanks so much for all these explanations. So this would mean that in some instances, capturing and replaying >20 kHz frequencies could create something different below 20 kHz, something unique for some ears... Apart from the handbells example, what other musical instruments could provoke such runaway high-frequencies? Flutes? And would such effects be confined to classical music, or other genres like jazz could also be affected by such phenomena?

@landroni: A C4 handbell sounds a roughly-262Hz fundamental; a C5 is an octave up from that, C6 is two octaves up, etc.  Mallmark sells handbells up to C9 (about 8KHz).  I can't think of any other instruments other than pipe organs or electronic synthesizers which allow a musician to play notes with a fundamental that high.  Since the harmonic richness of a pipe is a function of its height/width ratio and high-pitched pipes are very short, I'm not sure how much predictable ultrasonic harmonic content the highest-pitch pipes have.

Interesting... And a related follow-up. As mentioned in the OP, Wikipedia says that "Sampling rates higher than about 50 kHz to 60 kHz cannot supply more usable information for human listeners, implying that reproducing frequencies of only up to 25 kHz--30 kHz could be useful for the hearing experience... And I suspect via the mechanism you are proposing: hi-freq waves combining to generate an audible low-freq tone. So in your opinion is there a reasonable upper-bound for such high-frequencies that could conspire to create aesthetically-pleasing low-freq content? I am trying to understand...

...whether, to capture most "useful" cases of intermodulation of ultrasonic-frequency content, the commonly used 96 kHz sampling rate is sufficient to cover such cases (capturing up to 48 kHz frequencies, well above the Wikipedia-suggested 30 kHz upper limited); or whether going to 192 kHz sampling rates (up to 96 kHz frequencies) is necessary. So would one need to play back 96 kHz or 192 kHz samples in order to potentially cover these higher-freq-generated and aesthetically-pleasing low-freq content? My intuition is that 96 kHz sampling is sufficiently ample to cover most such cases...

I would suggest that, given a 96kHz recording, it should be possible to produce a 44kHz recording aesthetically indistinguishable from the original by applying a tiny amount of distortion or other processing before down-conversion, but the kind of processing required for best results might vary depending upon the nature of the original sound.  If an individual would perceive a 96kHz original as aesthetically superior to a "straight" 44kHz conversion, some combination of processing parameters would probably yield a 44kHz file the person would consider to be better yet.

If one knew in advance exactly how to configure the microphone and recording, it wouldn't be necessary to record at 96kHz; the advantage of recording at 96kHz would stem from the fact that one could experiment with parameters in post production and then yield a result essentially equivalent to having recorded at 44kHz with exactly the right parameters.

We're drifting far more into music/recording issues than biology, however.

Absolutely. Thank you so much for all the wonderful explanations! To revert to biology, from what I hear, the bottom line is that adult humans do not hear above 20 kHz. But it is perfectly conceivable that ultrasonic waves interact to generate audible content (below 20 kHz). This is likely to be very subtle, and to vary from one individual to another. This is an incredible insight, that may or may not validate the need to record and play back at higher sampling resolutions (e.g. 96 kHz).

Taken from "24/192 Music Downloads... and why they make no sense":

Sampling rate and the audible spectrum
I'm sure you've heard this many, many times: The human hearing range spans 20Hz to 20kHz. It's important to know how researchers arrive at those specific numbers.
First, we measure the 'absolute threshold of hearing' across the entire audio range for a group of listeners. This gives us a curve representing the very quietest sound the human ear can perceive for any given frequency as measured in ideal circumstances on healthy ears. Anechoic surroundings, precision calibrated playback equipment, and rigorous statistical analysis are the easy part. Ears and auditory concentration both fatigue quickly, so testing must be done when a listener is fresh. That means lots of breaks and pauses. Testing takes anywhere from many hours to many days depending on the methodology.
Then we collect data for the opposite extreme, the 'threshold of pain'. This is the point where the audio amplitude is so high that the ear's physical and neural hardware is not only completely overwhelmed by the input, but experiences physical pain. Collecting this data is trickier. You don't want to permanently damage anyone's hearing in the process.
The upper limit of the human audio range is defined to be where the absolute threshold of hearing curve crosses the threshold of pain. To even faintly perceive the audio at that point (or beyond), it must simultaneously be unbearably loud.
At low frequencies, the cochlea works like a bass reflex cabinet. The helicotrema is an opening at the apex of the basilar membrane that acts as a port tuned to somewhere between 40Hz to 65Hz depending on the individual. Response rolls off steeply below this frequency.
Thus, 20Hz - 20kHz is a generous range. It thoroughly covers the audible spectrum, an assertion backed by nearly a century of experimental data.

Above: Approximate equal loudness curves derived from Fletcher and Munson (1933) plus modern sources for frequencies > 16kHz. The absolute threshold of hearing and threshold of pain curves are marked in red. Subsequent researchers refined these readings, culminating in the Phon scale and the ISO 226 standard equal loudness curves. Modern data indicates that the ear is significantly less sensitive to low frequencies than Fletcher and Munson's results.

This seems to imply that it's highly, highly improbable that anything above 20 kHz could be heard by the human ear, and that in most realistic conditions even that threshold would never be reached. I'm curious if others more knowledgeable can confirm or contradict this...

Yes, perhaps 10% of humans can hear up to 28 kHz, if it's loud enough:

Ashihara K. Hearing thresholds for pure tones above 16 kHz. J Acoust Soc Am. 2007 Sep;122(3):EL52. doi: 10.1121/1.2761883. PMID: 17927307.

Hearing thresholds for pure tones between 16 and 30 kHz were
measured by an adaptive method. The maximum presentation level at the en-
trance of the outer ear was about 110 dB SPL. To prevent the listeners from
detecting subharmonic distortions in the lower frequencies, pink noise was
presented as a masker. Even at 28 kHz, threshold values were obtained from
3 out of 32 ears.
Absolute thresholds for pure tones have been studied by many groups of researchers. The absolute threshold usually starts to increase sharply when the signal frequency exceeds about 15 kHz. It reaches about 80 dB SPL at the frequency of 20 kHz. Above 20 kHz, however, only limited data have been reported. According to recent studies, ultrasounds seem to be inaudible as long as their level does not exceed about 85 dB SPL.
The present results show that some humans can perceive tones up to at least 28 kHz when their level exceeds about 100 dB SPL.

Many people who think they've heard higher than 20 kHz are actually hearing intermodulation products or aliasing in poor-quality audio systems, though.  Typical speaker systems have nonlinearities that can cause spurious tones.
The linked paper confirmed that this wasn't due to subharmonics, though, so 28 kHz is a real world limit.


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Metrics to analyze branch lengths in phylogenetic trees
I'm interested know about some basic metrics that could be used to discriminate trees based on their branch lengths. I know of branch length unaware topological/tree shape-based methods such as Colless and Sackin's indices and am curious whether there are similar metrics that utilize branch length to discriminate. For example, the two trees below have an identical topology but are very different.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, this question seems like it might be a better fit for [Bioinformatics.SE]. (Note: please don't repost your question to that site — instead request migration). Thanks!

Thanks @tyersome! This similar post elsewhere on this site brought me here.

You're welcome! Bioinformatics.SE didn't exist 4 years ago, so that isn't really a good indicator of what is currently a good fit for this site ...

Are you essentially asking how to interpret the difference in the two phylo trees(that is,given the tree,what do you conclude),or are you asking which tree to produce for your data(that is,given the items,which tree to produce)?The horizontal length gives you a sense that two things are very separate or not.Looking at the second tree,you could say that right at the beginning of time,d,e,f differentiated but a,b,c remained identical until some much later date when they finally split and differentiated.The horizontal distance doesn't have to be time-any measure that measures similarity will do.

There are a variety of measures of tree similarity implemented in the TreeDist R package. (Your phylogenies appear to be from the R ape package, so hopefully you are somewhat familiar with R.)
Other tools include treedist from Joe Felsenstein, which computes Robinson-Foulds and the Branch Score Distance (which sounds closely related to your interests, described in this paper). You can see that software page for a lot more information.
For a practical description of the different tree comparison metrics you can see this article.
I would suggest taking a look at the manual and the multiple vignettes associated with the TreeDist package to learn more about how exactly those metrics work. There appear to be a wide variety of metrics in there that I have never heard of, such as clustering entropy or split entropy or Nye similarity.
This package also includes tools for making visualizations of differences, such as that shown below:

I don't know whether this is actually used in phylogeny, but if you restrict the problem to cases where the topologies are the same, each tree can be described as a point in a n-dimensional space where n is the number of branches, and each axis represents the (possibly normalized) length of one of the branches.
You can then compute distances between points (i.e. trees) in that space.

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How does a sheep's fleece impact its tolerance for high temperatures?
I am interested in whether a sheep endures more stress when its environment is hot if it has a full fleece or if it is recently shorn.  Put another way, at the extremes, is a sheep more likely to die due to high temperatures if it has its fleece or if it does not?  If the answer depends on breed, what are the biological differences that cause one breed to interact with this element of its environment than others?
I am interested in temperatures around 90°F but if the answer differs at some temperature commonly experienced somewhere on Earth, that would be interesting to know as well.
I am interested in modest relative humidity values, in the 40%-60% range, but again if the answer differs outside of that range it would be interesting to know about.
I considered asking this question on a physics stack exchange (where a sheep might be modeled as, say, a radiator with or without insulation) but I'm particularly interested in the answer for real, actual sheep - biological processes and all - and not just a spherical sheep of radius r.

Wool serves as a good insulator, meaning it doesn't allow warmth to escape the wearer easily allowing the wearer to remain warm. Furthermore, wool helps maintain a dry environment by absorbing moisture from the air (and sweat) which can also keep you cool during summer.
Here's a link that talks more about this for both wool wearers and sheep: https://shepherdsdream.com/blog/wonders-of-wool/how-wool-keeps-us-cool/

Thanks.  Wicking seems like a really good point.  I had the impression that sheep don't sweat but https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1365279/pdf/jphysiol01094-0027.pdf apparently contradicts this notion.

Yeah, there are only a handful of mammals that have some form of perspiration.

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Why the major gene model can be supported by finding de novo mutations in affected cases?
I found a sentence which I can't fully understand in a publication on the genetics of autism.

The unified major gene model is supported by the significant increase
  in damaging de novo mutations found in subjects with ASD as compared
  to their unaffected siblings.

Is it saying under the major gene model, the de novo mutations comprise the majority of genetic risk?

It helps to give context and a source citation in questions like this. With some research I identified the source of the quote as Torre-Ubieta, "Advancing the understanding of autism disease mechanisms through genetics".
The quote comes from a section of the paper discussing the main two different genetic models of ASD: (1) the polygenic (many genes contributing small influences) model, and (2) the major gene model, where a variation of a single gene is responsible. The first two sentences of the paragraph having the quote are:

The unified major gene model62,63 is supported by the significant increase in damaging de novo mutations found in subjects with ASD as compared to their unaffected siblings44,49. Further support for this model is seen in the phenomenon that there are more inherited SNVs that disrupt protein function in conserved genes transmitted from the mother to individuals with ASD than in unaffected siblings73.

The sentence in question (the first) is simply citing evidence supporting the second kind of model; it is not claiming that the majority of risk is due to de novo mutations.  As to how de novo mutations support the major gene model, it helps to consult the papers cited in the sentence.  Review of citations 44 and 49 show that those with ASD often have rare de novo mutations that look to be gene-disabling, whereas their unaffected siblings do not.  This suggests that disabling of a single gene can bring on ASD, and thus fits with the major gene model, but does nothing for the polygenic model since it supposes one gene difference has only small effect.
Let me add that the two models are not mutually exclusive: a polygenic model might explain the observed familial occurrence of ASD, while a de novo major gene model might explain why only a few in a family are affected.

Thanks a lot for your detailed answer! I'll do better in posting a complete question with context or reference next time. I was confused yesterday because I didn't figure out the reason why the evidence raised in the sentence I cited can't support the polygenic model. Now it's much clearer after your explanation.


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What is multiplet nuclei capture rate?
I met this terminology in a publication.https://core.ac.uk/download/pdf/226940818.pdf.
It's in the last sentence of the second paragraph in the text.
I tried to search for it but didn't get a conclusive definition.
Is it an important parameter whiling processing snRNA-seq data?

It is multiple nuclei capture rate. They talk about it in the supplementary section near the bottom of the article. They diluted the processed sample to get an estimated 2000 nuclei per microlitre. They then want the machinery to process individual nuclei, but cant tell from the results if two or more nuclei are processed simultaneously (which would give a mixed signal). That's why they estimate the multiple nuclei rate using a separate experiment with nuclei from a mix of mouse and human cells.


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Have Bonobos and Chimpanzees competed?
After reading de Waal's "Our Inner Ape", I'm left with the impression that chimpanzees would easily drive away or kill-off bonobos, if they were to compete for the same territory.
Have there been any instances of that in the wild? Or have their habitats always been completely separated by the Congo river?


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How can just new born baby can walk ?
This website here stating video of New born baby walking breaking the internet.
How can just new born baby can walk ?

The baby isn't walking exactly. It can't support it's own weight. It's stepping: moving its feet in a step-like fashion when the tops of the feet are brushed against a surface or placed on the surface, a primitive reflex like the Moro Reflex, present in all normal newborns.

@anongoodnurse are you saying website is wrong?

@GerardoFurtado - I've tested every newborn I've delivered or taken care of, and I have to admit this one is impressive, if only because 1) the baby is being held aloft so long and effortlessly by the...person, and 2) the baby usually gives up after a few 'steps', at least, I gave up then, as the point is not to see how long they can do it, but that it's there. So, all in all, it's a fun vid. Don't rag on the midwife. I would have commented as well, and I've seen it hundreds of times.

@DhanrajKumar - I didn't say anything about the video or the website. You see what you see. I'm explaining what is happening.

@GerardoFurtado - Well, then, I agree with you. It's for the camera, I guess.

@GerardoFurtado - That makes sense. I don't understand Portuguese (wish I did), but it sounded to me like an excited grandma ("Oh, look at what my beautiful, talented, miraculous new grandchild can do!" kind of thing. Nice of the midwife to give grandma such a sweet treat for posterity. (Grinch that I was, I would have been more concerned with getting the baby dried off/warmed up.)

@GerardoFurtado - Don't honestly know. Still has a lot of vernix (caseosa) on it. Lots of it wiped off. Could be a few hours, yes.

@DhanrajKumar- http://www.techtimes.com/articles/208562/20170529/watch-video-of-newborn-baby-who-tried-to-walk-immediately-after-birth.htm

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text:
What is the name of this plant I found in ROAD HIGHWAY?
Location of the plant is South India,
Plant stem looks like Banana.

Down vote, why so?

@AScientist thank you for detailed suggestion, can you give me advise where else I can post this pic to get its ID.

I don't know if any botanist can identify it with only this image. I think you should see this to write a standard identification question. https://biology.stackexchange.com/questions/59005/streamside-plant-identification-oregon

I don't know why @DhanrajKumar your post got down vote. he provided nice quality picture & also I know the answer to your post.

It is Fishtail Palm, Example picture look like this:

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text:
what is this mushroom and how to grow this mushroom?
What is this mushroom?

And how to grow this?

If I knew how to grow this particular mushroom, I would start a side business doing exactly that. They are very marketable.

Please add the location the picture is from

i find this in my village forest  in india himanchal pardesh kinnaur purbani

SEARCH "MOREL CULTIVATION", it is difficult, technical, requires good rainwater / special water and good microclimate, and it's low production quantities. some people cultivate morels. experienced pickers can find many of them in certain places. its interesting. the best thing is to put them in blender with other ingredients and throw all the spores everywhere shadey rainy and well drained. i found this vid for example https://youtu.be/lTFugHA2WaI?t=310

Regarding how to grow it, try https://gardening.stackexchange.com


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Book about ordination in ecology
This is a question I posted on Cross Validated few weeks ago but no response has been given so far.
I am looking for a book that would cover a lot of different ordinations techniques (indirect gradient analysis e.g. PCA, CA, DCA, MDS, nMDS but also direct gradient analysis e.g. CCA, CCorA, RDA) with applications in ecology (with R would be better) and mostly focusing on these methods.
I think " Numerical Ecology " by Legendre & Legendre (https://www.elsevier.com/books/numerical-ecology/legendre/978-0-444-53868-0#) would be relevant but it seems to cover a very extensive number of topics. Any other idea ?

I took a class in ordination methods a few months ago and found the following books helpful in better understanding the various techniques:
Multivariate Statistical Methods: A Primer by Brian Manley https://www.crcpress.com/Multivariate-Statistical-Methods-A-Primer-Fourth-Edition/Manly-Alberto/p/book/9781498728966
Correspondence Analysis in Practice by Michael Greenacre (this is somewhat more in-depth for forms of CA) https://www.crcpress.com/Correspondence-Analysis-in-Practice-Third-Edition/Greenacre/p/book/9781498731775
Multivariate Statistics for Wildlife and Ecology Research by McGarigal, Cushman, and Stafford https://www.springer.com/gp/book/9780387988917
Numerical Ecology is really excellent, even if it covers a broad number of topics. I focused on the ordination methods and found it to be very straightforward. Check out the McGarigal et al. book if you are interested in seeing examples of application in ecology.

You might also want to consider:

Tree diversity analysis by Kindt and Coe 2005. Freely and legally available here. Not very deep but nice and crisp introductions + its free.
Numerical Ecology with R by Borcard et al. 2018;
https://link.springer.com/book/10.1007%2F978-1-4419-7976-6
Little brother of Legendre and Legendre 2012. Excellent book with many examples in the R language. Also very up to date as it was released this year.
Analyzing Ecological Data by Zuur et al 2007; https://www.springer.com/us/book/9780387459677. Also a nice book covering the basics of ordination in ecology.


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Sleeping Pill Overdose
How does an overdose of sleeping pills kill?
What are the body's reactions to an overdose?
In an article published in ScienceDaily, I read that "Sleeping pills owe half their benefit to the placebo effect".
So what constituents of a sleeping pill, when taken in excess, lead to a negative reaction?

Note that "Sleeping pills owe half their benefit to the placebo effect" is a statement about the efficacy of placebo for helping sleep; it says little about the actual effects of the drugs and does not mean that sleeping pills are just placebo and does not mean they do not have physiological effects.

Some hypnotics — the active component of sleeping medications — act as central nervous system (CNS) depressants, which in turn depress breathing or respiration, especially when mixed with other drugs, such as alcohol.
If your breathing slows sufficiently and is arrested, as can be caused by an overdose of CNS depressants, your vital organs will be starved for oxygen, which in turn can lead to brain damage and — ultimately — death.

(+1) Piggybacking to say you'd have a vicious cycle of respiratory depression reducing blood oxygen saturation, causing ischaemia and poor perfusion in the respiratory centre (RC), killing the neurons there and in turn causing more respiratory depression. At some point, when all your RC neurons are dead, you stop breathing completely. This would be after the death of other areas of the brain due to the extensive blood supply of the RC. Also I'd note that most hypnotics depress the CNS by facilitation of GABAergic transmission.


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Isn't it an evolutionary disadvantage to have a single organ perform so many essential functions?
This is in reference to the human liver, responsible for not only the production of bile, but also the filtration of blood, metabolization of drugs, detoxification and so on. Liver failure is often synonymous with death. So how exactly did the liver come to perform so many essential functions, with no backup whatsoever?

While the liver is vital, I don't know why you consider it more of an evolutionary failure than many other organs. One would die without a working heart (heart failure), kidney, gastrointestinal tract, brain, lungs, etc. Maybe you can clarify your question a bit. Also, metabolism of drugs/detoxification are basically the same thing, and filtration of blood also occurs in the spleen (its major function). Thanks.

The brain performs many essential functions, although it's more like a "division of labour" type of grouping, like in a factory where everything happens in specific rooms... we could have many small livers and brains and gonads all around the body, although evolution has decided to group everything together pretty much since the early bilateral animals. What is weird is that the skeletomuscular components of arthropods and vertebrates are totally symmetrical, and the rest is totally assymetrical.

Yes, but splitting it up into multiple organs is also a disadvantage, becasue you have to grow and upkeep said organs. every solution has its pros and cons that have to balanced.  Most of evolution is lesser of two evils compromises, kluges, or "good enough" solutions.


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Schizocoely and Enterocoely
In terms of phyla, mollusca, annelida and arthropoda are schizocoelic, whereas echinodermata and chordata are enterocoelic.
I know that their difference lies in the formation of the coelom but how exactly is enterocoely more advanced than schizocoely?

Neither is "more advanced" than the other, they are separately evolved mechanisms to form a gut.
You may be misled by a human-centric view that treats humans and animals more humanlike as more advanced or "more evolved" than other animals but this is not true: all life has been evolving for the same length of time.


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How close are we to having phages take over the role of infection control from antibiotics? What developments need to occur?
The discovery of, and research in, the field of phages was overshadowed by the discovery and implementation of antibiotic treatments for infectious disease control.  With the rising concern of antibiotic-resistant microbes, is there a serious effort to refocus research and development to master the science and technology of phages?

Welcome to Biology.SE! This is a good first question. I suggest you to make the tour in order to learn more about this site and earn yourself your first barge. Have a good stay!

This is a very interesting topic. Indeed, historically, it might seem that "phage therapy" research is in a dormant state. But there are some groups actively doing theoretical research on the synergy between phage treatments and the immune system, as well as research on how the appearance of antibiotic resistance could be attenuated by the use of phages.
Nevertheless, this research is not what the field is trending towards, since there is still hope to find new antibiotics (for which, then, we will see other types of resistance evolving), and most of the funding agencies are still privileging this instead of the alternatives.
A colleage of mine is working on this very same theme. Here is one of his recent research papers on a specific type of infection.
Cheers,
Pedro


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Trying to make a homogeneous phantom
I am making a T1 weighted phantom for an MRI project. It consists of distilled boiling water, 7g/L agar, 10g/L NaCl and 1g/L CuS04. As the phantom cools it will get a jelly like texture. What I would like is for the phantom to be as homogeneous as reasonably possible when it solidifies. What do you think is the best way to do so?
I was thinking of having the mixture on a vibrating plate, or maybe a centrifuge or even just inverting the mixture at regular intervals. Any ideas would be greatly appreciated.

I don't know what a weighted phantom T1 is but having used soft agar I do know that 0.7% agar is extremely sloppy, sort of semi-solid. If it is present as a thin  layer on top of a standard 1.5% agar plate and you jerk the plate then the top layer will deform. This is with microbiology-grade agar, maybe less pure versions behave differently?

Hi Alan, that's from a recipe I saw before. But I've looked at other recipes and they say 2.3% which seems a lot more realistic! Thanks for confirming my suspicion!


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Why does closing one eye in bright light allow me to open the other?
I often find it physically painful to open my eyes past a squint after stepping out into the full summer sun. However, if I close one eye entirely, I can keep the other open without pain. This seems odd. Naively, one would assume the pain results from too much light entering the eye and doing some sort of damage to the interior, but if this were true, closing one eye would have no effect on the other. Does the fact that it does imply the discomfort is actually related to (e.g.) the sum-total of information reaching the optic chiasma?

Not an answer but an addition to your question. Might help to achieve better results. As far as I can remember I have always closed my left eye in bright light. I am right eye dominant. This is in Indiana which is not extraordinarily high in UV light. I went to Guam recently and I found I could not open either eye without extreme discomfort. Guam is notably high in the UV spectrum. Sunglasses were a must at all times. I am Caucasian with blue eyes. In the latitude of Indiana I have not had extreme discomfort as in Guam but have had to close my left eye more than enough. As a Biologist, I hope

I do not think that there's any scientific reasons why, but it is like a reflex. Your brain knows we do not enjoy bright light in the morning, especially when the eyes weren't open for a long mather of time. It is why peeking slowly to give time to your iris to get adapted to the strong light. Some people open one eye at the time, some people opens both of them and blinks repeatedly.

I thought of this same question today. Wish there was an answer!

A couple of factors play into this. First, you're halving the number of nociceptors that are signaling the brain. Second, there is a psychosomatic effect. Your brain continuously combines the visual data from both eyes to form one image. With one eye closed, your brain combines the brightness of both inputs to form an image that is roughly half as bright as reality. As a result, your brain not only ignores a portion of the nociceptor signals from the open eye, but it also doesn't assume the presence of pain like it normally would.
I've no publicly accessible sources to cite, as this is something I learned in my EMT class. Someone actually asked your same question in class

your right eye is dominant making it a reflex to close the other which in this case is your right eye which is the "Weaker" one

Just A guess Sorry :(

If you could add some references, and expound, that would be good :)

This happens to me as well. Complete guess (and probably somewhat of a poor answer) but I think it has something to do with focusing problems (similar to an extreme astigmatism) jerking the eye muscles around.
Closing 1 eye removes the need for a coordinated focus, eliminating the problem.


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What is this row of pits along the "upper lip" of theropod skulls?
Consider the row of pits visible in the "upper lip" area (and to some extent, the "lower lip" too) of this T-Rex skull at the Palais de la Découverte, Paris (picture from Wikipedia):

I noticed similar pits in a Deinonychus skull a few weeks ago when I visited the American Museum of Natural History in New York:

What are they?

They are called Nutrient Foramen which are innervation of blood vessels and nerves, you see the same thing in reptile and bird skulls (mammals tent to pack it all into one or two large openings). They feed blood vessels and nerves to the gums, lips, and face.
Dinosaurs do seem to have more of them, but size making them more noticable is also a factor. The increase in dinosaurs may be involved with pressure sensitive scales as seen in crocodiles or alternatively something like lips, or both. Here is a great article on them. Paleontologist are hampered here becasue the related animals are birds (who have beaks) and crocodiles (which are entirely scaly). So it is hard to pin down exactly what a dinosaur oral facial anatomy would look like.

Excellent; and great link!


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What's the difference between prions and prion-like proteins?
If I added a prion domain to a protein, does that make the protein a prion-like protein or would it be considered a prion at that point?
I'm trying to understand what prions are, how they aggregate and what macroscopic shapes they conform to (i.e. a ring vs smaller micelles).
Thank you very much!

My understanding is that the principal quality of a prion is that it behaves like a prion in cells- the logic is a little circular.
A few of these criteria for acting like a prion (in yeast, where prions are most common):

Reproduces itself by "templating" (refolding of non-prion versions of itself into prion versions)
Sensitive to protein denaturing agents (which get rid of the prion protein conformation).
Dependence on protein chaperones which reproduce prions by releasing prion oligomers from larger prion aggregates. These oligomers go on to "seed" new prion aggregates.
Forms insoluble protein aggregates consisting of many copies of the prion protein.

An important subtlety here is that proteins with identical amino acid sequence can be both prion and non-prion in the same cell. It is a biochemical consequence of a specific protein structure, rather than simply a feature of the protein sequence. Thus, a prion domain confers the ability to become a prion, not necessarily "prion-ness" itself. This Scientific American article might be helpful regarding this point.
As an example of how these criteria are applied, this paper uses some biochemical and genetic methods to screen for the presence of new prions in wild yeast.
As a review of how prions oligomerize and form their classic aggregates, this paper might be helpful.
It is certainly true that creating fusion proteins with candidate prion domains is a common way of confirming that those domains are competent to become prions (see e.g. this paper). But there is usually a higher standard of evidence to show that some protein actually is a prion- usually by demonstrating the existence of heritable protein aggregates mentioned in point (4).
Hope that helps.


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Will charged water ions sprayed onto plants keep insects off?
I had stumbled on an article about a Dutch firm that devised an irrigation system that used mist of ionized water droplets that they claim keeps insects away from the plants.  This break through would revolutionize eco-friendly organic agriculture by reducing the need for insecticides.  They also claim nitrates are also formed by the process and embedded in the mist to supply nitrate fertilizers as well.  Thus eliminating the need for extra chemical fertilizers.
I tried to find the site again and the company but not coming up on search.
Are there any merits to these claims?  How would such a process or device work?


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Is amphibians being descended from fish reflected in the animalia taxonomy?
I think it is common knowledge that amphibians are descended from fish. At some point there was a transition from sea to land.
But when I try to confirm this through the Animalia taxonomy, the scientific classification of fish goes

https://en.wikipedia.org/wiki/Fish
while the scientific classification of amphibians go

https://en.wikipedia.org/wiki/Amphibian
If we draw this as a tree of sorts, we end up with

it seems to be quite obvious that fish and amphibians belong to the same phylum but different clades, but I'm not sure how that proves that amphibians are directly descended from fish?
I'm interested in a tree that shows amphibians branching off of the fish lineage.

Look in to the difference between cladistics and phenetics/phylogenetic trees.

the phylogenetic trees i found only went as far as animalia, if were looking for fish or amphibians. so i was hoping cladistics would be like another focused phylogenetic approximation of the animalia kingdom, are they not related?

They are related but not the same. If you read about them it's easy to find comparisons of how they differ.

Your "tree" is drawn incorrectly. What you have labeled as ancestors and descendants are nested groups. Vertebrates and amphibians are both chordates, and amphibians are also vertebrates. The wikipedia taxonomy box uses outdated, non-phylogenetic terminology.

Fish are a paraphyletic group: that is, any clade containing all fish also contains the tetrapods, which are not fish. For this reason, groups such as the class Pisces seen in older reference works are no longer used in formal classifications.

You got something completely wrong. In evolution one can not say that one taxonomical group evolved from the other. We say that two taxonomical groups have common distant relative. With that said all vertebrates have common distant relatives. Important is to know when did the branching in speciation happened.
Proto-amphibians evolved in Devonian by further speciation from relative that was sarcopterygiian (fish). It was a fish with some properties of amphibians (lungs and bones in appendages).

From:
https://en.m.wikipedia.org/wiki/Rhipidistia

Can you please put a source for your quote and the phylogenetic tree?

are you trying to say that all amphibians are fish but not all fish are amphibians? If that is true I don't understand how you cannot logically conclude that amphibians have to have evolved from fish, without making any inferences about intermediate transitory forms?

"The first major groups of amphibians developed in the Devonian period, around 370 million years ago, from lobe-finned fish which were similar to the modern coelacanth and lungfish." <- this is the language from wikipedia that led me to believe amphibians evolved from fish

@notacorn Yes, what you said is exactly how it works. Amphibians, as well as reptiles, mammals, and birds, are technically a type of highly modified fish. They don't stop being fish just because they are highly modified from the ancestral form. Some fishes, such as lungfish and coelocanths, are more closely related to amphibians and reptiles than they are to sharks, bass, or other fishes.

@notacorn I think that Domagoj's point is that "fish" is not a very useful grouping in the first place. "lobe-finned fish" is a slightly more useful classification, as it's much more specific.

Maximillian is correct "fish" is a not a useful term, it is polyphyletic by most usages, the closest useful term would be vertebrata

Check through the classification of lungfush:
under a cladistic view, tetrapods are themselves considered a group within Sarcopterygii
https://en.m.wikipedia.org/wiki/Sarcopterygii
And
https://en.m.wikipedia.org/wiki/Rhipidistia


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Where can I find free authoritative images of different species of Lagomorphs?
I would like to make an infographic showcasing the order Lagomorpha (rabbits, hares, and pikas), which contains a dozen genera and about 100 species. I want to include a picture for most species, or, failing that, a picture for each genus. The difficulty is that I'm not at all an expert on these animals -- I just find them cute and I like infographics -- so if I simply google around for pictures of them, I won't be able to verify that a picture labeled "Bunolagus monticularis" is actually a picture of a Bunolagus monticularis specimen, rather than something else.
Photographs would be ideal, but I'm fine with using sketches instead when no photographs are available. It would also be ideal if the images were free to use and in the public domain (or licensed under some version of Creative Commons)
Is there any source for images of species specimens that is generally considered trustworthy? It's fine if it's limited to lagomorphs, but if it also extends to other animals/plants, that's all the better!

Wikipedia is good for this,
The licence is what you want, and many people will have checked the animal ID.
look up the two pika species, and the rest are under
http://en.wikipedia.org/wiki/Leporidae

Good answer. I actually just finished another project like this (an infographic about foxes) using Wikipedia for images, and although I'm also not an expert on foxes, I did sort of have the feeling that it was probably trustworthy. I'll come back and accept this answer in a couple of days if there isn't a better one by then.


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How to grow bacteria?
We have this science experiment on how to grow a bacteria, our teacher told us to use gelatin, beef stock, and sugar as an alternative for agar. I am confused on  why we need gelatin, beef stock, and sugar in growing a bacteria. What ingredient is in those 3 materials that can aid in growing bacteria?

There are several requirements for bacteria to grow.

A carbon source - Sugar
A nitrogen / amino acids source - Beef stock
Gelatin is there to hold everything in place, it doesn't provide any nutrients.

Everything that lives needs food to grow. That food may be as simple as nutrients needed to build parts to more complex tasks like storing and/or converting energy.
Different bacteria require different things. A nutrient source like beef stock contains lots of amino acids and proteins which can feed a large spectrum of bacteria.
Sugar is a densely packed energy store that many bacteria can use for powering biologic processes.
Gelatin is a mixture of peptides and proteins which adds even more nutrients to the system. More importantly, its thick gelatinous structure acts as a binding agent/ substrate which keeps everything from sloshing around in the dish (which can be very inconvenient when moving it around).
In short the simple petri dish is about providing a wide variety of nutrients so that it can support the growth of a wide variety of microbes.

You know you could just edit it for a point that small


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What Genus Is This Ant Queen?
I believe she is either Lasius or Formica, but I am an amateur so thanks for any help. This queen is completely black and gray, with a gaster that kind of looks like the stone Tiger Eye but gray. There is no red or brown on her. She’s approximately 1.5 cm long and I found her in central Minnesota. She laid eggs overnight after being caught. I know the photo is terrible thanks to my phone but it was the best one I got of her.


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Preprocessing microarray data to detect increased male expression variance due to dosage compensation?
I am currently working with a dataset from a large microarray experiment where one of the aims is to look for evidence of the predicted doubling of variance in expression on the X chromosome in hemizygous males relative to females due to dosage compensation.
Speaking broadly, the experiment uses a controlled breeding scheme in Drosophila to generate individuals that are heterozygous or hemizygous for different known X chromosomes (the autosomal genotype is also controlled). I then want to use a genewise linear modelling approach to estimate additive genetic variance for gene expression for each gene in males and females. The arrays involved are Affymetrix GeneST arrays.
My initial inclination was to preprocess the array data using RMA, in my case from the oligo package in R. A fundamental part of RMA preprocessing implementations is a log2 transformation, and of course this has desirable properties for most gene expression analyses. However, it is apparent that the variance-stabilizing properties of the transformation have some undesirable consequences when looking for the sex differences in expression variance across samples that I am interested in. A toy example showed that variance in log2 expression is the same whether or not males show dosage compensation, obscuring the very signal I am interested in.
I would like to retain the benefits of the preprocessing steps (e.g., background correction), but I wonder if anyone can weigh in on the best way to avoid the log2 transformation’s effect on estimates of variance. Is it appropriate to simply take the antilog of the expression matrix after RMA preprocessing or is there another approach/package I should look into instead?

I would probably be able to answer if I knew what exactly the "expression matrix" contained, and exactly what you take the logarithm of. In general, I would need to know exactly what information you have, and what the algorithm does. If you don't get an answer here. It may be your best bet to go to Cross Validated Stack Exchange and ask. Although, they would not need to know all the biology you've written here, and like I, they would need more precisely what data you have, and you want to achieve mathematically.


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How did fig tree take root in trunk of palm tree?
Please see pictures below.

I never saw anything like this.  Do the roots of the  fig tree penetrate the trunk of the palm tree?  Is there a symbiotic relationship between the two?

Ok, so first of all, that is a fig - more specifically, it's Ficus carica, which is commonly grown for its sweet fruit. Secondly, the palm is most likely Phoenix canariensis, a palm which tends to accumulate a thick layer of dead and decaying leaf bases around its trunk, which then can break down enough that plant seeds can grow in them. The town where I live has several of these palms growing in the main street, and at least two have plants growing up in their old leaf bases like that.

how t ofruit seed get most places, hint it's poop. animals poop in many places.


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If mantis shrimp have 16 photoreceptors then how many other colors on the spectrum are there?
Mantis shrimp have 12 to 16 photoreceptors and humans have 2, and in rare occasions even 3. But if mantis shrimp can see 16, how many other colors are out there? How many photoreceptors is possible? How much of the spectrum is not ever going to be seen by any creature ever?

Some sources - http://phenomena.nationalgeographic.com/2014/07/03/natures-most-amazing-eyes-just-got-a-bit-weirder/        https://en.wikipedia.org/wiki/Mantis_shrimp     https://phys.org/news/2013-09-mantis-shrimp-world-eyesbut.html

Not really answerable, since color is a subjective term.  I suppose an upper limit would be in the Xray or gamma part of the spectrum, where photons become energetic enough to destroy receptor molecules.  Some aquatic creatures sense electric & magnetic fields, so it would be theoretically possible to detect radio wavelengths: https://en.wikipedia.org/wiki/Electroreception

Related for your final sub-question: https://biology.stackexchange.com/questions/57708/what-is-the-biological-potential-for-vision-of-wavelengths-outside-the-human-vis

The first source you posted pretty much answers your question. Here are some others, probably referring to the same study but talking about it differently:
The Mantis Shrimp Sees Like A Satellite (National Geographic; this article is referred to in your first source)
Study Offers Insights into Unique Color Vision of Mantis Shrimp
Mantis shrimp's super colour vision debunked (Nature)
Here is the paper that those three articles are based on:
A Different Form of Color Vision in Mantis Shrimp
And what seems to be the author's (slightly more recent) thesis on the subject:
Colour vision in mantis shrimps: understanding one of the most complex visual systems in the world
The big thing to understand is that there is no such thing as "the color spectrum". There is the electromagnetic spectrum, which is one-dimensional: you can describe an electromagnetic wave's position on the spectrum with one number, its wavelength. But if you look at a picture of the electromagnetic spectrum with the colors associated you can notice something immediately:

You don't see a uniform increasing of a single quantity from one number to the next, you see several distinct colors following each other.
That's because the point of color vision isn't to detect variations along the electromagnetic spectrum per se; the aim is to allow our brains to get more information about the world around, based on the fact that light comes in many different wavelengths. Different objects will reflect different combinations of those wavelengths, meaning being able to tell some of those wavelengths apart improves our ability to tell objects apart based on those differences.
The key here is that there isn't a perfect way of doing this; nobody has a system where you detect the exact wavelength of each photon and tell exactly how many of each wavelength you receive. What human eyes do is have some specific receptors be more receptive to some wavelengths than others, and then the brain compares how excited each receptor is and puts all that information together to generate a sense of "color", which is basically a way of telling some things apart when they reflect certain different wavelengths. It's related to wavelength, but isn't the same thing; for example our brains recognize wavelengths that excite the red and green receptors equally as "yellow". This includes wavelengths that fall between the red and green wavelengths, but also combinations of red and green wavelengths. That's how you get the color wheel, the ability to make some colors out of others, and the fact you can generate all colors that we see from three primary colors. An organism with an extra receptor between the red and green would be able to tell those different combinations of wavelengths apart so that "yellow" to us would look like several different possible colors to them. Conversely, trichromatic humans are able to tell colors apart, like red and green, that are one single color to dichromatic mammals.
So the answer to "how many colors on the spectrum are there" is "there is no universal color spectrum". Every organism with its own system of light receptors can theoretically have its own color spectrum; how many colors they see is a question of how many different combinations of wavelengths they can tell apart, and that's a function of how many receptors they have but there can also be other factors (like the sensitivity of given receptors, how much processing power they're dedicating to color vision, exploiting different aspects of physics that affect wavelength... In humans even language and culture can influence color discrimination to some extent).
And where does the mantis shrimp come in? Well this is interesting, because it's been generally thought as you put it that the mantis shrimp would be able to see many more colors than we do, due to its much more numerous receptors, but the recent studies mentioned in the first source you linked to suggest that the mantis shrimp is worse at discriminating colors than we are, i.e. it sees fewer colors. However it appears its color vision functions very differently, and that's where the 16 different receptors come in. It's possible that the different receptors allow the mantis shrimp not to detect more colors, but to process the colors it does detect much faster. To quote the Nature article:

If the shrimp eye compared adjacent spectra, like the human eye does, it would have allowed the animals to discriminate between wavelengths as close as 1–5 nanometres, the authors say. Instead, each type of photoreceptor seems to pick up a specific colour, identifying it in a way that is less sensitive than the human eye but does not require brain-power-heavy comparisons. That probably gives the predatory shrimp a speed advantage in distinguishing between different-coloured prey, says Roy Caldwell, a behavioural ecologist at the University of California, Berkeley.

And the National Geographic one:

Their working hypothesis is that the mantis shrimps analyse the outputs from all of their 12 receptors at once. Rather than making comparisons between those receptors, they pass the entire pattern of outputs onto the brain, without any processing. “One could imagine that they have a look-up table in their brain,” says Marshall. So rather than discriminating between colours like we do, their eyes are adapted for recognising colours.
“Oddly enough, the closest device to stomatopods would be a satellite,” says Marshall. “Remote sensing algorithms have look-up tables of colour to fill in the image that the satellite forms.”

For your other questions:

How many photoreceptors is possible?

Theoretically the limit would only be how many you can pack in an eye and how many chemical pigments exist, but in practice there is a trade-off between color and spatial discrimination (after all any color receptor is a light receptor that's limiting itself to certain wavelengths only, so you lose in overall light perception). Another article in the Science journal the article on Mantis shrimp color vision appeared in suggests the optimal number is isn't over 4 (in organisms that use our system of color vision of course, not the mantis shrimp's):

In fact, theory predicts that two to four receptor types are optimal for discriminating the spectra of natural materials and maximizing the number of objects that could be distinguished by color.

And:

How much of the spectrum is not ever going to be seen by any creature ever?

Again, considering every set of photoreceptors leads to its own color spectrum (and every brain probably cooks it to its own sauce beyond that), that question applied to the set of all colors isn't really meaningful. The answer would probably be along the lines of "almost all of it" because the set of actual color vision systems in the natural world is an infinitesimal percentage of the set of theoretically possible color vision systems... but it's not like those colors are "out there to be seen" in anything but the most abstract sense; they exist in the same sense that a child that's the combination of a sperm and egg that haven't met exists.
If by "spectrum" we mean "electromagnetic spectrum", then there is likely an upper and lower bound to the wavelengths that can be detected, where wavelengths on the upper bound are too deadly for a cell to survive let alone detect (though bodies can and do sacrifice cells to exploit inhospitable environments, see the cells lining our stomachs, so even that might not be an absolute obstacle), and on the lower bound aren't energetic enough to cause pigment molecules to react to them. I don't know what those bounds are though; it's likely that more important constraints are how useful it is to detect those higher and lower wavelengths, that any organism would bother evolving the ability. (also, for the lower wavelengths, whether their detection is associated with forming an image. For example we can detect infrared radiation as heat but we don't think of that as "seeing". On the other hand "eyespots" that detect visible light without forming an image are often thought of as a primitive form of sight; there is a level of arbitrariness there but it's also true that lower wavelengths have different optical properties).

"You don't see a uniform increasing of a single quantity from one number to the next, you see several distinct colors following each other." That is simply an artifact of the computer process used to make that image, likely in sRGB, which has far less of a color range than Adobe RGB or ProPhoto. Using a larger color space and having a monitor capable of displaying it would would produce a gradient with no human discernible steps to it.

@AMR it's not a question of discernible steps (in fact the previous image I had for this didn't have such visible ones but it was https), it's a question of yellow not being perceived as a shade of red or blue. Compare with one-dimensional entities that are perceived as one-dimensional (if not linear), like temperatures from warm to hot, sound from quiet to loud, luminosity from dark to light...

Then your answer is not explaining that point correctly. Electromagnetic waves are not one-dimensional. They have amplitude and frequency as well as wavelength. All of these contribute to the energy of that photon, which in turn excite electrons in opsins that can then create an action potential that causes the neuron to fire. The number of conjugated bonds determines what range of wavelengths the opsin will respond to. You are also making assumptions that I am not sure you can back up, and you should avoid doing that. You could add as a comment or clearly label that it is your opinion.

@Rozenn Keribin: But I do percieve the yellow grdually transitioning to orangish-yellow, then orange at one end, and greenish-yellow then green at the other.  And I dare say any interior decorator worth his/her salt could put at least a couple of dozen names to various shades in the transition: peach, tangerine, chartreuse, &c.

@jamesqf, AMR: these points should be discussed in chat I think. https://chat.stackexchange.com/rooms/60137/discussion-of-question-if-mantis-shrimp-have-16-photoreceptors-then-how-many-oth

@AMR I created a chat room to discuss this if you wish https://chat.stackexchange.com/rooms/60137/discussion-of-question-if-mantis-shrimp-have-16-photoreceptors-then-how-many-oth

@Rozenn Keribin: But alas, you can not create a functional chat.

@AMR There is no meaningful distinction between frequency and wavelength for EM waves, they are merely inverses of each other describing the same property. Photoreceptors are excited by single photons, so there is no meaningful distinction with energy, either. The only meaning of amplitude in terms of EM radiation is number of photons.

@jamesqf: it doesn't work? Can you create one?

@jamesqf : well ok then... I never said the colors don't gradually shade into each other, the point is that there are several different basic colors involved. Blue shades into green shades into yellow shades into orange shades into red, and in that spectrum we might call "peach" a shade of orange, but we won't call green a shade of orange. Compare with a white to black spectrum, where all shades in between are considered shades of gray, belonging to one overall transition.

@AMH: "Then your answer is not explaining that point correctly." -- Clearly so, and thank you for pointing it out; if I think of a better way of explaining I will change the answer. -- "Electromagnetic waves are not one-dimensional." They aren't, but the electromagnetic spectrum which is what I was talking about, is a representation of the variation of electromagnetic waves along one dimension - wavelength/frequency (as Bryan Krause points out those are two measures of the same quantity).

@Rozenn Keribin: You misunderstood me.  I didn't mean that chat doesn't work, in the sense that it appears to function in the manner its designers intended, I meant that it's basically useless to try to use it to hold any sort of discussion.

@jamesqf and comments are better for that? Or you didn't intend your comment to be part of a back-and-forth in the first place? I don't understand what you are saying at all.


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Sample suggestions for phase contrast microscopy
I am a non-bio student working on an academic paper recently and would like to have some sample preparation for phase contrast microscope.
For it to work, I imagine the sample to be:

Transparent;
Easy to obtain from daily stuffs;
Easy to slice and prepare (i.e. approachable to people untrained in bio).
Best dimension around 10 micros, and is well seen under x100.
Preferable to be seen dynamics at room temperature.

My current thoughts are:

Human: oral cheek cells, red blood smear, sperm.
Plants: onion surface cells.
Others: yeast, pond water.

Any further suggestions (especially dynamic ones)? Thanks!

Since phase contrast microscopy is a rather old technique, you might find a book on microscopy with sample preparation protocols in the library of your institution. And here a protocol from the web https://www.education.ie/en/Schools-Colleges/Information/Curriculum-and-Syllabus/Senior-Cycle-/Syllabuses-and-Guidelines/lc_biology_support.pdf

@fabianegli Thanks for the helpful link. Though I would prefer easier ways (instead of following the protocols) to prepare the samples, so as to save time and funding. The samples are for demo usage, so protocols are beyond sufficient.

Do you want to prepare the samples at the time of the demo or should they be stored days/weeks/months/years before the demo? Dynamic samples are normally wet samples and they have to be prepared fresh. For demo purpose, I would not take any body fluids, since you work with glass (danger of cutting the skin, including oral cheek skin) and the combination can pose a serious rick for infections. Also a blood smear is looked at when it is dry and would thus not be dynamic.

@fabianegli Thanks for the reply. The samples should be prepared at the time of demo. That’s exactly the reason why I would like an “easy-to-obtain” sample, especially for the dynamic ones. For now I have already tried on blood smear and oral cheek skin, they look good! However I should still need some suggestions for dynamic samples.

Any green, soft leaf from a non-toxic plant is a good start. Cut a thin slice from the leaf (either to look at the cross-section or the surface). Try different leafs with different colors - there might be colors in the cytosol and/or in chromoplasts.
Concrete example for dynamic structures:

Elodea leafs: they consist of only two cell layers and can be looked at under the microscope without further preparation. Keep the the leaf in water and cover it with a cover slide before looking at it under the microscope and add water when it starts drying out. The green chloroplasts in the plant cells are moving around as long as the cell lives.

You might find Elodea either in a pond or in a store selling aquarium fish and the like. You can keep Elodea alive and grow it in nutritious water at a sunny place.


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How does DNA determine all of our hereditary traits?
It's my understanding that DNA codes only for protein synthesis. Does that mean that hereditary traits, like the shape of our nose, are determined only by the proportions in which various proteins are synthesised in various parts of our body ?

DNA does not only code for proteins. Other products (e.g. non-messenger RNAs like microRNAs or ribosomal or transfer RNAs) exist. Also, DNA has further functions aside from protein-coding. Many DNA regions are regulatory, bind transcription factors, affect the topology of chromatin, host modifications, and much more. Lastly, it's important to be aware that hereditary traits can also be non-DNA-based. There is a very active field of research called epigenetics. Worth reading about!

"only for protein synthesis". those are bold words for someone built from proteins ;-)

Sure, but I am wondering what makes my nose stick out one way more than an other, when the instruction manual only indicates the local proportions of various proteins I am made of.

Does that mean that hereditary traits, like the shape of our nose, are determined only by the proportions in which various proteins are synthesised in various parts of our body ?

Yes, more or less!
A trait that is called heritable is a trait which variance in the population is in part at least explained by genetic variance. Most of these heritable traits, however, are also affected by environmental variation (and other sources of variance). For more information, please have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?
So when you say

[..] are determined only by the proportions in which various proteins [..]

The term "only" is a bit misleading. Other sources of variance exist that will affect the variance for this trait. However, it is a pretty good approximation to say that the heritable information is conveyed via the transmission of DNA and the phenotypic expression of this DNA is mediated via proteins.
We refer to the DNA -> RNA -> protein having some phenotypic impact relationship by the term central dogma of molecular biology. You might want to read more about it or maybe have a look at an online course such as this one from Khan academy for example. You will want to know the terms translation and transcription.
Now, in reality DNA can affect an individual's phenotype by means other than proteins (or polypeptides to keep it more general) that are synthesized from it. Indeed, many loci (locus=position on a chromosome) affect the expression of other proteins, others are translated into RNA but not transcribed into proteins (e.g. rRNA, tRNA, RNAi, ...) but yet still have an important action on a cell's physiology.


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Will DNA nanostructures be useful for medical applications?
There is a lot of work being done on developing small nanomechanical structures and even small nanomechanical actuators built with DNA.  I have heard researchers motivate this research with claims that it could have biomedical applications.  My question is, how likely is this to be true?  In particular, a few potential problems bother me:
(1) What is the risk that the foreign DNA strands used to build nanomechanical devices will be accidentally incorporated into the host genome?  Are there plausible strategies for avoiding this?
(2) Will it be effective in the presence of an immune system?  If the foreign DNA is not incorporated into the host genome, it seems likely to instead be destroyed by the host immune system.  Is there research addressing this issue?

"My question is how likely is this to be true." Which defines the question as a request for subjective opinions of the type that are off topic — see here.

@David If you look at the rest of the question, you see that I then clarify two particular questions.  I am not a biologist, and am asking (1) what biological mechanisms (if any) pose might accidentally incorporate foreign DNA floating around and are there any known possible strategies for avoiding this? and (2) Does the human immune system attack foreign DNA floating around inside the body?  Are there ways to prevent this?  I apologize if these seem to be subjective questions to an expert, but to me (a beginner), they are as specific as I know how to make them.  Thanks

I think biomedical applications are not an absurd perspective. More specifically, regarding your concerns:
(1) Unless the DNA is first internalized by cells, and then somehow enters the nucleus (both are not very likely, especially considering the small concentrations we're talking about here after dilution in a human body), you would still need the DNA structure to disassemble to become "available", and the strands to be long enough to be incorporated, which is usually not the case. And, of course, you would need some DNA integration mechanism to be at work, such as a recombination with genome sequences that happen to be very similar to the ones used to build the DNA nanostructure (which can be avoided during the design step). In other words, no, it's quite unlikely.
(2) Immune responses might actually be a bigger issue; in particular, some Toll-like receptors (TLR), that activate the innate immune system, can respond to DNA and RNA fragments. But immune responses may not be so problematic if the DNA nanostructures are used for short-term mission, like 1-shot delivery to a specific organ, in which case they do not need to stay around for very long. Additionally, this can be a useful feature; immune recognition can be used to direct the trafficking of nanoparticles to lymph nodes for example, where the efficieny of their payload (e.g. an immune modulator) could be maximized.


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Genomic library preparation: Why does the restriction enzyme not cut into the gene?
I am currently trying to understand creating a genomic library more profoundly. In most textbooks I read (as well as wikipedia), they mentioned that the genomic library is created by isolating the DNA and fragment it with a specific restriction enzyme that cuts approximately as many times as there are genes. However, that cannot really work, can it?
Let's say E. coli has 4000 genes with a 4,600,000 bps genome. That means I must generate fragments of more than 1150 bps in theory (if each gene is the same length and no other sequences are present). That would mean I need a restriction enzyme that cuts about 4000 times creating over 1150bps fragments. So I would either use a restriction enzyme with a recognition site of 5bps (cuts every 1024bps) or with 6bps (cuts every 4096), of course just if the base-pairs are random.
Now you already see, with the first restriction enzyme I will (even in theory) cut through many genes, while with the second I might get genes of the appropriate size but I will also fragment others.
Furthermore the genes, especially in more complex organisms are not spaced out equally, but may be concentrated in some areas, while in others just repetitive sequences are located.
So why does every textbook mention that I can create a full genomic library with one restriction enzyme? Wouldn't it make more sense to shear many copies of DNA randomly, just as it is done for shotgun sequencing, to get a higher coverage?
So my question is, how is a genomic library REALLY prepared without knowing anything about the sequence? Do you just take into account that much genes will be cut in the middle and hope for the best? It seems like a very weird strategy to amplify complete genes.
Thank you! :)

A genomic library is generated for the purpose of encapsulating the full genetic component of an organism.
You do this by fragmenting the genome with  restriction enzyme that cuts at its recognition sequence. These fragments are then taken and cloned into a plasmid, so that they can then be sequenced inside the plasmid using common sequences that are found on the plasmid but not (generally) in the organism itself. The sequencing would traditionally be performed by Sanger sequencing, which has a limit to how long a sequence you can do at once - really good sequencing will get you ~1000 bp, with sequence quality tailing off after about 600 bp.
The genomic library are not intended for expression - once genes are identified, they can be sub-cloned into an expression plasmid to see what they do. So for this purpose, cutting a gene into fragments isn't a problem, as you will find the rest on another plasmid and can re-construct the full-length gene by taking the two fragments and assembling them.
The reason you use the restriction enzyme is that the sequence that it cuts at is also used for inserting it into the plasmid.
So, at this point you might be asking yourself how do you match the ends of genes (or any sequence for that matter), when they are all cut by an identical sequence?
Well, the answer that is that you use multiple restriction enzymes, either by themselves or in combinations to generate a variety of fragments cut at different sites. This will mean that once you create the libraries from these different digestions, you can sequence through the different libraries and find where the fragments overlap, and then assemble all the sequences together into the original sequence.
For instance if you look at the picture below. If you imagine the the black boxes  are the same gene, and the in the top one is cut with restriction enzyme A and the bottom with B, you can see that the two restriction enzymes generate overlapping fragments, so if you sequence the fragments from both restriction enzymes, you can find where the ends in A match others in A, by looking at the fragments in B.

Thank you!!
So I guess genomic libraries are mostly used for sequencing, whereas cDNA libraries are used for expression (since you always get a full gene), which makes sense.
It really confused me, since in many "general" textbooks, they explain, that creating a genomic library is used to e.g. find a gene - which I associated with "they want to express that gene later". I didn't quite understand why you would want a fragmented gene. But I guess it makes more sense now. Thanks!

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Does aerobic exercise increase the incidence of disease via free radicals?
Aerobic respiration produces ROS, atleast one of which (the hydroxyl radical) cannot be neutralized by any known antioxidant and is always damaging surrounding tissue. I know ROS plays a role in signaling, positive feedback loop for growth/adaptation to increasing mechanical stress.
Increasing aerobic respiration through aerobic exercise (i.e. running) produces more and more ROS. Wouldn't this then increase subcellular damage and increase the risk of disease, as compared to somebody who is sedentary?


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Does interspecies breastfeeding occur in the wild?
Does interspecies breastfeeding occur in the wild?
Say, for example, a zebra feeding a wildebeest, or a bushbuck feeding a gazelle.
There is a Wikipedia page on this topic but it only shows animal-human and human-animal feeding.
https://en.m.wikipedia.org/wiki/Human%E2%80%93animal_breastfeeding

Not specifically "the wild" but pet cats and dogs have been known to nurse wild animals or other pet species, possibly inadvertently. There are several YouTube videos of cats nursing baby raccoons, for example. I'm unsure if they're aware the animal they are nursing is not a kitten or if they can't tell the difference.

Yes, interspecies adoptions have been observed. They're rare enough that study is limited to case reports, and the causes are guessed at but not fully understood. However, I think it's clear that there are strong biological drives towards participating in mothering for the species that do so, and it's not too surprising that these drives could be at times "misplaced" from a biological perspective and directed at non-offspring.
A couple papers:
Carzon, P., Delfour, F., Dudzinski, K., Oremus, M., & Clua, É. (2019). Cross‐genus adoptions in delphinids: One example with taxonomic discussion. Ethology, 125(9), 669-676.
Izar, P., Verderane, M. P., Visalberghi, E., Ottoni, E. B., Gomes De Oliveira, M., Shirley, J., & Fragaszy, D. (2006). Cross‐genus adoption of a marmoset (Callithrix jacchus) by wild capuchin monkeys (Cebus libidinosus): Case report. American Journal of Primatology: Official Journal of the American Society of Primatologists, 68(7), 692-700.

I didn't ask for adoptions, but specifically breastfeeding. Has this ever been recorded? If so, between which animals?

@Samid Read the papers in the answer. They involve breastfeeding. Do you think these animals would otherwise get milk from the grocer?

@BryanKrause while your comment is true, it'll be more proper as an answer to the question if you include at least the word "breastfeeding" in your answer :)

This video describes a cat feeding ducklings, and shows the ducklings subsequently still having the emotional attachment to their foster mother even after growing up.

Not "in the wild" and the ducklings didn't breastfeed.  The bit at the end about the lioness may qualify.

@JamesK: They did breastfeed; it was clearly stated that they were observed to be sucking at the nipples. Even though it's on a farm, one could argue that cats are kind of semi-wild, and there is no reason to believe that the same thing couldn't happen in the wild. No doubt the quality of evidence provided by this is low, but it's worth knowing.


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What is the end-point of material from an apoptotic cell, after phagocytosis?
Apoptosis occurs. The organelles and interior material form apoptotic bodies that are packed in vesicles. The cell membrane breaks apart (cell no longer exists) and apoptotic bodies enter the extracellular space. Phagocytes "eat" the apoptotic bodies.
What happens then?
Is the material processed again and effluxed into the blood, sent to other cells, ...?