text:
What kind of hot pink eggs are these?
I saw a dozen or more clusters of what I think are insect eggs attached to a few vertical sticks protruding from a small pond, and a few more to stalks of grass nearby. Location is in Hsinchu County, Taiwan, end of March, fairly good weather these days in the neighborhood of 15-22 C.
Each cluster consist of a group of roughly 150 spherical hot pink colored eggs stuck to a surface, each about 2.5 to 3 mm in diameter. One group was deposited almost completely around a stalk of grass on land next to the pond, and several others were deposited on the side of a stick from a fallen branch sticking out of the water.
Questions:

Is it possible to identify what kind of insect produces such clusters of eggs?
Is there any explanation possible for the "hot pink" color? I suppose it could be a general "don't eat me" signal like these big juicy red bugs but it's such an artificial looking color, I've never seen it anywhere in nature, at least that I can remember.

click images below for full size:

update: This answer suggests that snails are the likely culprits, and so I returned to the scene of the crime today and caught them red-handed, or in this case "pink-footed".
Click for full size; the larger snail is about 5 centimeters in diameter.

 caught red-handed, or in this case "pink-footed"

Great post that received a great answer!! :). +1 to both!   I've closed as duplicate due to a very similar post from Singapore a year ago. I think linking these 2 posts in this way is most efficient for site bookkeeping. However, if you think that your post and/or species is sufficiently different and maintaining your question as a unique post is useful, then I could possibly be persuaded to reopen. (though, again, I think linking as dupe works best).

@theforestecologist I'm all for keeping all our pink egg questions in one basket ;-) Based on the answer I revisited the pond a few hours ago I took some much better photos of the snails there which are likely the culprits. I was going to accept the answer and then post a supplementary answer with them, but maybe I will just update this question with two more photos. Since it's now closed and it complements rather than complicates the existing answer, does that sound okay?

I think making a clearly "Updated" portion of your answer with photos of the snail species is appropriate. However, if you think your new info/photos suggests a different species than the one suggested in the previous answer, I'd be happy to open the post back up -- a unique ID to species is reason enough to let you post a unique answer :).

@theforestecologist I've added the additional snapshots above and left a message under (at)tyersome's answer. I'm no expert but it certainly looks like these are those. Thanks!

Those appear to be the eggs of a species of apple snail in the genus Pomacea, probably the introduced invasive golden apple snail (Pomacea canaliculata), but there are at least two other candidates1,2.
You can learn more about this species and the problems it causes from this Columbia University webpage.
For comparison — Figure 3 from "The identity, distribution, and impacts of non-native apple snails in the continental United States"3.

Egg masses of introduced and native Pomacea in the continental U.S. a. P. haustrum, b. P. diffusa, c. P. canaliculata, d. P. paludosa, e. P. insularum. Scale Bar:5 cm.
References:
1: Yang, Q. Q., Liu, S. W., He, C., & Yu, X. P. (2018). Distribution and the origin of invasive apple snails, Pomacea canaliculata and P. maculata (Gastropoda: Ampullariidae) in China. Scientific reports, 8(1), 1-8.
2: Yang, Q. Q., & Yu, X. P. (2019). A New Species of Apple Snail in the Genus Pomacea (Gastropoda: Caenogastropoda: Ampullariidae). Zoological Studies, 58(13).
3: Rawlings, T. A., Hayes, K. A., Cowie, R. H., & Collins, T. M. (2007). The identity, distribution, and impacts of non-native apple snails in the continental United States. BMC Evolutionary Biology, 7(1), 97.

Wow, thank you! I never would have imagined that those were snail eggs. I don't have a close-up but I did notice that the pond is full of small snails. Below the big image there are two smaller images that will display full size when clicked. If you look at the one on the left there are dozens and dozens of snails at the bottom of the pond and there are snail trails everywhere. I don't suppose it's just a coincidence. This is probably not the first invasive snail I've posted here either! What are these four large snails doing?

Type "b" looks like eggs of the variety in the aquarium trade in the US.  I found they needed to have a very humid atmosphere to hatch.

Thanks again for your answer! I've revisited the pond and took some photos of the snails in proximity to the eggs. Apart for being covered in algae the do seem to match the shape of the "golden apples" though in this case with the algae they look more like green apples!


text:
Is there a surface or body cavity that does not have epithelium?
Is there any surface in the (human) body that is not covered with epithelium?

Can you narrow down what you mean by "surface"? It might matter.

@kmm - It doesn't matter, really.

I don't know if I'm missing the point but I thougt that there is no epithelium on the surface of the teeth and the joints.

@mioppli nobody seems to be refuting this - I'd post it as an answer, maybe.

Are you referring to body cavity in the medical sense of the term (https://en.wikipedia.org/wiki/Body_cavity) or something more colloquial like e.g. a skin fold? (Asking "in the body" sounds like you mean the medical sense to me.)

Short answer
Edit with credits to anongoodnurse: As far as I know, every bodily surface and cavity is covered by epithelia.
Background
Epithelial tissue is a sheet of cells that covers a body surface or lines a body cavity. There are two types of epithelium in the human body:

Covering and lining epithelium forms the outer layer of the skin; lines open cavities of the digestive and respiratory systems; covers the walls of organs of the closed ventral body cavity.
Glandular epithelium surrounds glandular tissue.

Hence, the entire the bodily surface is covered by some sort of epithelium. Even the eye is covered with squamous epithelia (thanks to anongoodnurse for pointing this out).
And while acknowledging that an absence of evidence is not evidence of absence, I believe that there is no surface on, or cavity in the body not lined with epithelium.

Fig. 1. Epithelial lining of bodily surfaces. source: Ternopil State Medical University

I wonder if there is any body cavity which is not connected with the outside of body and also it doesn't have epithelium.

@SepehrM Depends on your definitions of "cavity" and "connected", I guess. I mean, would the ventricles of the brain count? They're full of CSF but typically described as cavities, and connected to each other but not to the outside (although this wouldn't answer your question directly, since they have epithelium).

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Why would hawk moths evolve long tongues for Darwin's Star Orchid when there are other flowers around?
Why would hawk moth evolve long tongues for Darwin's Star Orchid when there are other flowers around? Also isn't it counter productive for some flower to evolve a long nectar tube as this would shift the pollinators to other plants?
This coevolution makes sense if the only source of food for the moth is this star orchid and the only pollinator for the flower is the hawk moth. But if we consider other species to also exist in the picture, this coevolution seems counterproductive to me. For example most flower evolve mechanisms to attract pollinators as their is competition for pollinators as well.

I think the key terms are niche and co-evolution;

Why would hawk moths evolve long tongues for Darwin's Star Orchid when
there are other flowers around [?]

Because the moths have grown a long proboscis as an adaptation to a certain niche. As you say, not much other species can feast on the flower's nectar, so it makes perfect sense to narrow your niche by elongating your proboscis, and reap the benefits of this little visited flower.
A niche is

[T]he range of environmental conditions in which a species can exist.

As the University of South Africa explains:

One important part of the idea of the niche is that it is controlled
by how the species exploits resources in its environment.  If there
are two species living together and exploiting the same resources,
then one will usually be worse than the other at doing this –
eventually, that species will disappear because the other species will
outcompete it. However, species can live together because they
exploit different resources or because they exploit the same resources
in different ways.  These species then have different niches, even
though they occur in the same place.

Then how would the flower benefit? Now I'm going a bit more into a hypothetical explanation, but flowers need cross-pollination to reproduce and genetic mixing. If a plant species can bind a certain pollinating species to itself, it can make sure that that pollinating species only forages on that particular species of plant. Hence, that plant species can ascertain that the pollinating species carries only the right pollen and therefore make sure the transferred pollen is from the same plant species. This is beneficial, as pollen from other species won't pollinate them.
It's all a matter of co-evolution, in this case of two mutualistic species, nicely and succinctly explained by the University of California, Berkeley:

The term coevolution is used to describe cases where two (or more) species reciprocally affect each other's evolution. So for example, an evolutionary change in the morphology of a plant, might affect the morphology of an herbivore that eats the plant, which in turn might affect the evolution of the plant, which might affect the evolution of the herbivore...and so on.
Coevolution is likely to happen when different species have close
ecological interactions with one another. These ecological
relationships include:

Predator/prey and parasite/host
Competitive species
Mutualistic species

The hawk moth Xanthopan morganii praedicta pollinates the Madagascar star orchid (Angraecum sesquipedale) with its long proboscis. source: Encyclopedia Briattanica

This hypothesis of binding a certain species increasing the chances of cross-pollination is really convincing!

Two other hypotheses might be that nectar and pollen come from different parts of a flower, so flowers designed in ways that make it harder to reach nectar may be better at transferring pollen, and that some pollinators are more effective than others due to their foraging habits or body structure, so visits from some pollinators are preferred over others. These are just generic, I don't know if either applies in this case.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Why should we preceed neostigmine by atropine in tubocurarine toxicity?
Why should we precede neostigmine by atropine in tubocurarine toxicity ?
I know that neostigmine act as anticholinesterase thus increasing the number of Ach molecules rendering them able to displace the tubocurarine, but I don't get the idea of atropine I know it's muscarinic inhibitor but we are speaking about nicotinergic receptors?

Please present your thoughts on the topic or at least an attempt at finding out the answer you seek. What are the actions and target sites of neostigmine and atropine?

I know that neostigmine act as anticholinesterase thus increasing the number of Ach molecules rendering them able to displace the tubocurarine , but I don't get the idea of atropine I know it's muscarinic inhibitor but we are speaking about N receptors

Tubocurarine is a non-depolarising neuromuscular blocking aqgent, that is, it acts as a competetive antagonist of Acetyl Choline at the Nicotinic receptors.(Toxicity/Effect: $-N$)
Atropine is a competitive antagonist of the muscarinic acetylcholine receptor, classified as an anticholinergic. (Effect: $-M$)
Neostigmine blocks acetylcholinesterase, increasing the concentration of ACh at, and stimulating both muscarinic and nicotinic receptors. (Effect: $+M+N$)
Hence, to counter the only nicotinic deficiency of ACh, we give Neostigmine, which will also stimulate the muscarinic receptors, leading to muscarinic side effects. To counter the latter, atropine is given. A similar formulation is used in a disease like Myasthenia Gravis, with a functionally similar lesion.
$$(+M+N)+(-M)+(-N)=0$$

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
How does this small brown crescent-headed land planarian(?) "look around" and sense its envirnoment?
This 2-3 cm long, thin brown worm with a wide "anchor" or hammer or crescent shaped head was seen in northern Taiwan slowly moving along a damp tile outdoor surface. It moved by contraction/extension and regularly lifted its head appearing to explore its environment, as if to say "where should I go next"?
Comments suggest that this is a land planarian.
Question: Is it possible to confirm that this is a land planarian and to understand what sensory organs it has on its head in order to "look around" and decide where to go next?

Related: https://biology.stackexchange.com/q/55054/16866

@theforestecologist yes, it does indeed look like a land planarian and the hammer-shaped head was my first clue, thanks! (see also here from here) So all that's left now is the part about how it senses its environment.

Edited to reinforce that this is not a duplicate because what's still asked here is the part about how it senses the environment

Given that "hammerhead worms" are Bipaliinae, I expect you can find your species from this bibliography1.  Bipalium or Diversibipalium ruteofulvum and cosmopolitan Bipalium kewense are mentioned, but I did not find images of these species online just now.
A paper about the sense organs of B. kewense (Abdel-Haleem, 2014) mentions many small pigment cup eyespots, as well as papillae and pits that may be chemosensory in nature.

1Kawakatsu et al. 2004 An Annotated Bibliography of Taiwan Land Planarians, with Lists of Linked Papers on This Animal Group

Thanks for your answer! The historical bibliography is intriguing, and also provides a historical view to the colonial rule period.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Do cochineals ("scale bugs") form aluminium complexes themselves? Where do they get such large quantities so quickly and how do they handle it safely?
Wikipedia's Carmine begins:

Carmine (/ˈkɑːrmən, ˈkɑːrmaɪn/) – also called cochineal (for the insect from which it is extracted), cochineal extract, crimson lake, or carmine lake – is a pigment of a bright-red color obtained from the aluminium complex derived from carminic acid.1 Specific code names for the pigment include natural red 4, C.I. 75470, or E120.
1 Dapson, R. W.; Frank, M.; Penney, D. P.; Kiernan, J. A. (2007). "Revised procedures for the certification of carmine (C.I. 75470, Natural red 4) as a biological stain". Biotechnic & Histochemistry. 82 (1): 13–15. doi:10.1080/10520290701207364

Wikipedia's Dactylopius; Cochineal dye includes the image below of a ~5mm individual Dactylopius confusus that's been squished and a finger covered in a bright red dye thereby "extracted" from it.
And my guess is that the central aluminium may in fact be necessary to produce such a strong absorption of green and blue light (λmax = 530–335 nm).
But it's not yet clear to me where the aluminum for complexing comes from. Is it in the insect's diet and the "aluminium complex derived from carminic acid" is performed inside the insect itself? If so, from where do these insects get their aluminum in such large quantities how do they handle it safely?

video: Why Tiny Cactus Bugs In Red Food Dye Are A $35 Billion Industry | Big Business | Insider Business

Question: Do cochineals ("scale bugs") form aluminium complexes themselves? Where do they get such large quantities so quickly and how do they handle it safely?
"so quickly" because they seem to be pretty short-lived and I'd expect that bio-available aluminum would be pretty scarce.
The reason I ask is because biological aluminum has a toxicity aspect and it doesn't seem to me that it's something you'd particularly get a lot of sucking on plant juice.

Click figures for full size. above first: "Figure 2. Salasaca dyer showing red woollen cloths with modified cochineal red colours. Ecuador. Photo: A. Roquero." from Ana Roquero (2008) Textile Society of America Symposium Proceedings Identification of Red Dyes in Textiles from the Andean Region above second: "Dactylopius confusus crushed scale insect, Fort Collins, Colorado, United States" from Wikimedia. below first: "scale bugs" on my houseplant, perhaps female Dactylopius confusus or Dactylopius coccus, from Are these little white fuzzy insects "scale"? What species and what is their lifecycle like? below second: Structure of carmine from Wikipedia

companion question: Are these little white fuzzy insects "scale"? What species and what is their lifecycle like?

I gather it's in the diet of O. ficus-indica which does the binding, but I can't pin down the mechanism. I'll give it more time tomorrow, see if there's anything more detailed to find on the topic.

Definitely something to do with the Al. You get 2 carminic acids to 1 Al and the colour of the carminic acid alone is not bright red, more a deep orange. See article here

@bob1 Interesting!

Interestingly ionic salts produce other colours - substitute Na and you get indigo/deep blue, K and Ca salts are red to purple (may also contain Al I though) and ammmonium is blueish red. I'm having difficulty finding anything about the salts without Al though.

@bob1 the article I've linked to about dyed wool describes use of wood ash and lemon juice to induce different color changes as well.

pH dependent I would have thought. Wood ash = potassium salts, though I guess others present too.

Aluminium moves within plants as a complex with ligands such as oxalate, malate, and citrate.
Plant cells also hide the aluminium (and other junk) in vacuoles. That is most likely the immediate source for the beetle.
Plant roots exude malate and citrate to neutralise aluminium before it poisons the roots. I got this from The role of solute transporters in aluminium toxicity and tolerance.
The toxicity of aluminium is greatly dependant on its form and what it is complexed with. The more "naked" the ion is, the more toxic.
The toxicity is pretty much confined to the roots, and gets more nasty if the pH gets down to 4.3. Once inside the plant it is usually complexed, and not a big problem.
An easily readable review article on toxicity is Aluminum, a Friend or Foe of Higher Plants in Acid Soils.

This is all really interesting and mostly new to me, thank you!


text:
How to tell the difference between adult male Golden Orb spider and a juvenile female of the same size?
I believe these are Golden Orb-weavers (Nephila pilipes). PHotos of large adult females can be found in Do these large spiders in Taiwan belong to different species? They are quite common in Taiwan (and a wide swath of countires).
Based on photos around the internet, especially inaturalist.org and Wikimedia commons the little red one seems to be more likely an adult male rather than a juvenile female.
But I don't know!
This female is about 20 mm; I don't think I've ever seen one below 15 mm in a web at eye level. It's not uncommon to see them at 50 mm long (just the body).
It's hard to estimate the size of the little red one because it was in a parallel web about 10 cm behind the female's, and the mosquitos were going crazy on my arms and legs so I didn't spent time to get them both in focus at the same time for comparison.
Question: But I'm curious, what DO juvenile female Golden Orb-weaving spiders look like when they are growing up? Are they always distinguishable from males of equivalent size when growing up?

I've used my brave extraterestrial friend "LOCK Jian" (LOCK小將) (1, 2) for scale:

Update!
Looking through photos from a few weeks ago (same hiking trail) I found another pair. This female was slightly bigger (maybe 25 mm) but the little red companion this time was in the same web.
What's notable is that this little red spider is all round and plump, not elongated and rectangular like the one in the first set of photos! I esitmate that it was a bit smaller, maybe 3-4 mm.


text:
How do different sensory stimuli differ in nerve signal?
Every day, we experience different types of sensory stimulus, like heat, pain, cold, etc. However, in each case, the transmission of the stimulus to the brain through the neurones is carried on in the same way: through propagated depolarisation and repolarisation in axons, while through the release of acetylcholine at the synapses.
So, how does the different sensory stimulus differ if they are transmitted the same way? (I mean to say that how does the nerve signals differ for two different kinds of stimulus?)
Let's put the question simply:
How do two nerve signals originated from two different stimuli differ? If they do not differ, then how does the brain differentiate between different nerve signals if they are all alike? How does it understand what nerve signal carries what message?

I think the short answer to your question is that the contents of different types of sensory stimulation are communicated to different populations of cells in the brain (note this transmission is mostly glutamatergic, not cholinergic). From there, the remaining associations and experiences derive from connectivity with other networks of brain neurons that result in different types of experience, based on the networks that those networks form and learned associations over development and a lifetime.
Computer analogies aren't always appropriate to understanding things about the brain, but maybe it could work out a bit here. How does a computer distinguish between input on your keyboard vs your mouse? On many modern computers, it is common for both to be connected with USB. The computer has some software that distinguishes between the different inputs - the brain has hardware that does the same.
Later on in the brain, or at a different stage in a computer program, those inputs can be mapped to functions that underlie experiences or functional outputs. Movement of the mouse can be converted to the movement of a screen cursor ("motor output"). Proprioception (the sensation of the relative position of the body from receptors in the muscles, tendons, and joints) can be combined with motor plans to create an error signal to move a particular muscle to match the intended movement.
Explaining any further than this probably requires entire textbooks of material, so I will leave it there.

Agree, this is a massive question, with many subsections of the brain to consider, e.g. the lateral geniculate nucleus for visual input, cochlear nuclei for auditory, not too mention touch/pain/temp that all gets bundled up in the spine. Anyway there's some extra google food.

This is exactly the area of study known as neural coding. The representation of information is not universal and differs for different modality, different stages of information processing, and what not. It's an active area of research.
That said, for the peripheral nervous system, the simplest code is pretty much rate code with label line. In other words, knowing which nerve fiber is firing what rate carries much of the sensory information. There are adaptation and some timing information if you look closer.


text:
Terminology regarding sensory receptors
I was recently asked the following question:

Compare the following pairs of receptors in the same
  sensory system. Include in your discussion:

The distribution in the
  sensory epithelium;
What kind of stimulus is effective in activating
  them;
Their physiological response properties, function and central
  connections.

Rods and cones
Pacinian corpuscles and free nerve endings

In particular, I was not sure what the sensory epithelium is. Is it getting at the fact that Pacinian corpsucles are subcutaneous, while free nerve endings are cutaneous and that cones are centralized at the fovea?
Alos, I am not sure what their "physiological response properties" refers to. Since they are receptors, would their responses just be the output (i.e. peripheral/foveal vision and vibration/pain sense)?

The distribution in the sensory epithelium indeed refers to the location of the different receptors. And indeed, you are also right that cones are concentrated in the fovea, and rods are mostly found more eccentrically in the retina (Kolb, 2012. I would say the free nerve endings are situated just below the epidermis, and the PCs in deeper layers of the dermis (Fig. 1). But check your notes on what your prof. wishes to hear about this.

Fig. 1. Skin receptors. source: Neupsy Key
The physiological response properties of receptors is not their output per se. It is the way they respond to stimuli, that includes their output, but also includes the sensation of physical stimuli through second messenger systems or otherwise, and eventually the output. Kolb (2012 goes into detail on the physiology of photoreceptors in quite some detail and for the physiology of touch receptors I would refer to Dougherty in Neuroscience online.
References
- Dougherty, Somatosensory Systems. in: Neuroscience online. University of Texas
- Kolb, Photoreceptors. In: Webvision. The Organization of the Retina and Visual System (2012)


text:
What is the smallest touch sensation that a human can feel?
What is smallest touch (pressure) sensation that a normal, healthy person (not hypersensitive nor insensitive) can feel on the palm of the hand?

@fileunderwater - of course it's all about population averages. However I do agree with daniel; there are still many variables left; static pressure thresholds differ from hose obtained by vibrotactile stimuli. Furthermore, sensitivity goes down from fingertips > palm > back of the hand

What happened to all the previous comments? They are hardly irrelevant to the current question. @AliceD, do you have any idea?

@AliceD My point was not that it is about population averages, but that the smallest sensation/stimuli that a person can feel is likely to differ alot between persons, so the question is ill-posed. And removing hypersensitive persons feels like an arbitrary cut-off, when sensitivity is likely to differ dramatically between "healthy" persons.

@fileunderwater - the other comments were dealt with and I'm afraid I might have flagged your commentfor deletion - too quick perhaps. But let me put it this way - in psychophysics there is always a huge variation between people. Detection thresholds are subjective - people draw their own threshold. I, for example, generate relatively a lot of false positives, because I tend to feel stuff that is simply not phsysically present (it may be present in my mind for sure). Other folks pick a more stringent threshold and only say 'Yes' when they are absolutely sure they are feeling it

Short answer
The detection threshold of static indentation stimuli on the palm of the hand is approximately 10 to 40 micrometers, dependent on the exact location under investigation.
Background
The sensitivity of a sensory system can be expressed as the detection threshold. This threshold is in psychophysics generally defined as that stimulus level where, on average, 50% of the stimuli are felt.
There are several types of touch receptors that can be investigated, each with specific types of stimuli that are associated with them (Fig. 1)
 Fig. 1. Skin receptors and their response properties (Delmas et al. (2011)
The question specifically targets detection thresholds of indentation stimuli. These stimuli are typically expressed as distance units (meters) or pressure units (Newtons). The skin indentation under constant force is dependent on the area of contact, skin type and other parameters of lesser importance. Hence, indentation units using distance metrics may be the most appropriate way of expressing static detection thresholds. Johansson & Valbo (1970) investigated static detection thresholds on the palm of the hand (Fig. 1) and found average thresholds of 10 to 40 micrometers indentation. This variation was due to geographical differences; towards the fingers sensitivity is higher and thresholds are hence lower (Fig. 2).

Fig. 2. Detection thresholds of static stimuli on the palm of the hand. source:  Johansson & Valbo (1970)
References
- Delmas et al. Nature Rev Neurosci (2011); 12: 139-53

Definitely seems like research that would've been done in the 70s :p. Anyways, nice answer! And interesting too!

I wonder if the number of false positives (or possibly the sensitivity) would change if the subject were first exposed to a video of fleas or other light-touch parasites. Or better, if they were exposed to live fleas jumping on them for a while...
I know that I definitely feel hypersensitive to microtouches if I feel I might be crawled on, and I understand that this is not uncommon.

@DewiMorgan personally, I check for false positives by including catch trials where  subjects are provided  with the regular visual cue for "stimulation is up", but no tactile stimulus is presented. A "Yes" answer is per definition a false positive. If the false positive rate surpasses the 25%, the subject is instructed to raise their internal subjective  threshold and the run is restarted.

@AliceD: Oh, I know it can be compensated for. I was just interested in whether the sensitivity or error rate changed with the same subject, according to mental stimuli like that.


text:
Would a shark whip into a frenzy from smelling its own blood?
Sharks normally respond very quickly to the scent of blood in up to a mile radius, but what if the shark itself simply got injured? Would it respond to its own blood at all?

That would mean the real question is: why not? How could they automatically distinguish their own blood from that of another shark or fish? Would simply knowing it got injured be enough?

Great question +1

I'm pretty sure, they can smell their own blood, but they do not attack themselves. Wounding a fish results in the release of chemicals into the water. This is a signal for other fish about potential danger and they will escape (Schreckstoff). Of course, the predator of the wounded fish will not mind. So this seems to work best within the same species. Fishermen and military have apparently used dead or rotten sharks in the past to keep sharks from attacking (Shark repellent). I guess, a similar mechanism plays a role here. Sensing a wounded member of the same or close species (including oneself), would block any feeding behavior.
The Myth Busters have actually done this (not very scientific) experiment: https://youtu.be/E1GenfKR9pk

It is likely not the case that there would be a feeding frenzy if the question is whether a shark would attack an injured member of it's own family or species. The main reason is for reproductive means as a video will explain on this website:
https://sharkopedia.discovery.com/shark-topics/life-cycle/#how-do-sharks-avoid-inbreeding
Although there could be a few exceptions.  Semelparity in female tiger sharks for instance, has been observed.  Information about all sharks pertaining to this matter is difficult to come by.

This doesn't answer the question, which is clearly about the response of a shark to its own blood.

The question is what if the shark itself simply got injured?  Would there be a freezing frenzy?  And the answer I'm suggesting is no.  The shark wouldn't eat itself for the same reason..

They prefer not to fight with members of their own species.

The question is Would a shark whip into a frenzy from smelling its OWN blood?  The first sentence of your answer incorrectly restates the question by ending thus; if the question is whether a shark would attack an injured member of it's own family or species. My initial comment was made so you knew the reason for a down-vote and could consider editing the answer.

Yes, sadly they do as the smell of fishes blood turns them into a frenzy, as they are fish.But i see no reason the shark would get hurt in the first place.


text:
Do Black Pepper and Black Nightshade share specific characteristics?
In my textbook, I read that two organisms of the same species share specific or fundamental characters. Piper nigrum (Black pepper) and solanum nigrum (Black nightshade) share the same specific epithet despite belonging to different families. Is this because they share common fundamental characters ?

On botanic, the scientific names are: monomial, binomial or trinomial, so having just one word, two words or three words (words attached together, and words attached with a hyphen are calculated as a single word).
So, from top to Genus (inclusive), we use only one word. So names should be unique, and taxa sharing the same name have some common characteristic (or better: a common evolutionary past). Note: there are few cases with same Genus name in botanic and in zoology, for a different genus. [On botanics, with the exception of Genus, looking at suffix of a name, gives you also the rank of such name. If you doesn't recognize and it is not plural, it is a Genus. Else it is unranked clade]
Then there are binomial names, just below Genus to Species. With exception  of species, where is an abbreviation which define the rank between the two names (e.g. subg., sect., ser.). The second name just specify the genus, so e.g. in Solanum nigrum, the nigrum specify which Solanum. Just the word has no meaning.
To be complete, there are also trinomial names (e.g. subspecies, varieties and forms): the first two part are the specie name (so binomial) plus an abbreviation of rank plus the detailed name. Also in this case it has meaning only together with the first two names.
You choose two species with nigrum, and luckily both had black berries. But it is not always so. Helleborus niger (niger is the masculine, nigrum the neutral) has nothing related to black, but if you dig the roots.
Often the specific epithet is about a botanist, and some time just to honour him/her, so there is no common characteristics on such plants sharing the same specific epithet.
Source: The International Code of Nomenclature: http://www.iapt-taxon.org/nomen/main.php?page=title and his companion book: The Code Decoded (where you see such exception and examples, but many of them are put as example directly in the ICN).

Thanks a lot for answering my question using nomenclature! It helped a lot :)

@KavyaChandrasekaran - thanking someone doesn't help; if the answer is helpful - upvote; if the answer sufficiently answers your question - accept it (arrows & check mark on the left of the answers above)

AliceD  thank you for pointing this out to me, I'm new to this site so I didn't know a couple of things. I shall learn from this :)

@KavyaChandrasekaran no worries. I'm just trying to help. Well done and feel welcomed.

Short answer
Nigrum is Latin for 'black'. As you write in your post, it's black pepper and black nightshade. Not until the level of Class and Phylum do they share the same taxonomic classification. Hence, the species suffix nigrum doesn't tell you anything about their kinships, other than their physical appearance (they're both black).
Background
In general, the species part of the linnaeus nomenclature has nothing to do with evolutionary relationships. Instead, it is the higher classifications that denote kinships, for example, as you already suggest, the genus name, that may have various related species in it (Fig. 1). The species you mention are of a different genus.

The Species: Piper nigrum belongs to the Genus Piper, Family: Piperaceae, Order: Piperales, Class: Magnoliopsida, Phylum (Division): Magnoliophyta, Kingdom: Plantae, and Domain: Eukarya
The Species Solanum niger belongs to the Genus Solanum, Family: Solanaceae, Order: Solanales, Class: Magnoliopsida (Dicotyledons), Phylum (Division): Magnoliophyta, Kingdom: Plantae, and Domain: Eukarya.

They share only the same Class (and hence Phylum, Kingdom, Domain). For comparison, in the Kingdom of Animalia, we have the Phylum Chordata (vertebrates), that splits up into the Classes Mammalia (Mammals), Actinopterygii (Bony Fish), Chondrichthyes (Cartilaginous Fish), Aves (Birds), Amphibia (Amphibians) and Reptilia (Reptiles). So your two plant species share as much in common at the taxonomical level, as Mammals and bony fish.
Piper nigrum (or black pepper), is a climbing vine in the Piperaceae (pepper family) native to the Malabar region of southwestern India. Black pepper is grown in various tropical regions, including India, Indonesia, and Brazil, as it is one of the most important spices in the world.
Solanum nigrum (or European black nightshade) is a species in the Solanum genus, native to Eurasia and introduced in the Americas, Australasia, and South Africa. It is also known as black nightshade, duscle, garden nightshade, Indian nightshade, garden huckleberry, hound's berry, petty morel, wonder berry, small-fruited black nightshade, or popolo.

Fig. 1. Linnaeus nomenclature


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

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

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

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

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

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

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


text:
What determines the maximum frequency limit that humans can hear?
I learned that the human ear doesn't hear sounds outside the range of 20-20,000 Hz.
I can understand that sounds below this range are so weak that they don't affect the ear.
But why do sounds above this range have no effect on the human ear?
The reason I'm asking is that I'm going to teach a class on hearing and sound waves, but I'm confused about the direct reason of the lack of perception of ultrasonic waves - is there a barrier in the ear or what is the direct case of blocking of hearing for these waves?

It is generally agreed that 20 kHz is approximately the upper human 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 suspected to determine the upper limit of audible sounds to 20 kHz (Hemila et al., 1995). Indeed, 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).
Others, however, have reported that it is not only the middle ear structures, but mainly the tonotopic organization together with the finite length of the inner ear (the cochlea) that determines the upper frequency range. In mammals, tonotopy arises from a number of components, namely (1) the spatially graded BM stiffness that determines passive tuning of the basilar membrane (BM) and (2) the active frequency tuning of the BM due to auditory-nerve fibers innervating adjacent inner hair cells that sharpen up the tuning curve. In turtles, however, tonotopicity results largely from (3) the spatial gradient of the electrical properties of hair cells. Whatever the mechanism, tonotopy restricts the audible frequency bandwidth by limiting the characteristic frequencies of the auditory-nerve fibers innervating the extreme apical (low frequency) and basal (high frequency) regions of the cochlea (Rechiro & Temchin, 2002)
Your notion that

I can understand that sounds below this range are so weak that they don't affect the ear.

Is partly inaccurate, because you mix up sound level and frequency. It is, however, also partly true, because (1) large-amplitude, low-frequency stimuli may become audible at high intensities due to the high-frequency tail of the frequency tuning of inner hair cells (Smith et al.,1987) and (2) because the human ear is most sensitive to mid-range frequencies, increasing the amplitude of low-frequency sounds through cochlear curvature can affects low-frequency hearing limits.
References
- Pumphrey, Nature 1950; 166: 571
- Hemila et al., Hear Res 1995; 85: 31-44
- Smith et al., AJA (1987); 29: 125-38
- Rechiro & Temchin, PNAS; 99(20): 13206-10
Further reading
- Can humans perceive sounds above 20 kHz?

Wow... that's informative... is there any diagram descriping those 3 steps ? - for my note I was taking about physical wave energy but I'm happy with your notice.. I think @Jakob discriped physically and you did physiologically but I can't imagine your description clearly

@Abd-ElazizSharaf which 3 steps?

stimuli - ear sensitivity factors - inner hair cells affect

@Abd-ElazizSharaf - I am unaware of such a diagram; I work in the field and have given courses on this, hence I know it from different sources, as cited above


text:
Does the Miller-Urey experiment explain the origin of life?
According to the Miller-Urey experiment, the early earth atmosphere could have supported the formation of amino acids. This could provide an explanation for the origin of life. However, I do not understand how life could have started from amino acids (or proteins) which do not self replicate. Certain types of RNA do self-replicate, and it is plausible how life could have evolved from there.
Does it matter if amino acids came before RNA if they did? Is it correct to assume that in the RNA world, life somehow learnt how to use amino acids?

This is a common question. I think the experiment and its conclusions are often misunderstood.
Originally, the null hypothesis was that the ingredients for life could not have come about spontaneously, from inert, inorganic molecules. There was no evidence of strictly physical, non-biological processes being able to produce compounds that were necessary for the proteinaceous life as we know it. In other words, abiogenesis was therefore not supported by any line of positive evidence... until the Miller-Urey experiment. The experiment showed that the ingredients could arise through plausible, natural conditions prior to the existence of life! It bridges the gap between inert, inorganic, non-biological, and the rich soup of complex molecules that would - arguably - be necessary for anything like abiogenesis to even be a consideration based on empirical observation.
Of course the presence of amino acids is not evidence for the abiogenic origin of life. Life is not protein nor amino acid alone. But demonstrating that complex biological ingredient chemistry occurs spontaneously in large abundance - that sounds like a great take-off point for an abiogenic origin of life! That's really all the experiment achieved. In its historical context, it is a very impressive discovery, but it is certainly not a complete explanation, merely something that makes myriad biochemical explanations possible (and perhaps even plausible!). Perhaps you can now better appreciate why it excited and continues to excite biochemists working on trying to understand the chemical origins of life. The Miller-Urey experiment is foundational.
As for the transition from RNA to an RNA-protein origin of life, I quote briefly from another answer elsewhere here:

Regarding the transition from RNA-only to RNA-protein world, peptides
function as cofactors for some ribozymes. Amino acids and peptides are
known to have existed in the prebiotic environment and have been found
in space (glycine has been found in comets, along with other 70 amino
acids).

The actual problem with this experiment is that the environmental conditions implied in it might have never existed on Earth - at least, this is what the geologists say.

The discussion about the historical validity of the conditions assumed in the experiment has been ongoing and rich and full of disagreement, even among experts; similar experiments have been performed with many adjustments since. It's worth taking a look into it if interested!

This is reaching back several decades, but has the Miller Urey experiment ever been replicated? I thougt not... am I mistaken? I'd love to know.

@anongoodnurse thousands of times, with thousnds of variations. Miller Urey is just the first such experiment which is why it famous. The wiki has a nice summary of follow up work https://en.wikipedia.org/wiki/Miller%E2%80%93Urey_experiment

@John - I didn't know that! Thanks!

Answers gets more precise but conclusions are far stretched.
Going from amino acids to proteins or peptides (small proteins) is an unsolved problem. In water where they are supposed to be stored, they cannot combine. Water molecule occupies the link necessary to produce a valid amino-acid chain by which all amino-acids are linked into a protein.
Also, it is well less known that some mechanism must protect amino acids from linking by side chains, which is tough to avoid, and destroys the achievement of a correct peptide or protein. Chemists know how to do it with specialized chemicals and specialized laboratory material.
Nobody ever described a simple chemical formula to bring correctly amino acid together to form proteins, from chemical material that exists in a pre-biotic world.
Needless to say, that in the four classes of the building block of the building block of the life, amino acid, nucleotic acid, sugars, lidips, nobody knows how to pre-biotically control chemistry to assemble more complex molecules. It is almost impossible to bring a correctly linked chain of nucleotic acid in proper order (they must be obeying precise linkage (links to 3' and 5' ends). Ribose that is part of it, has still no explanation for its coming into existence in a prebiotic world.
The idea that time helps all this by failures and restart is misleading. Misaligned molecules (which is so highly inevitable) remain as they are. Source material is lost. Accumulation of chemical impurities impairs the success of having something useful. Delicate molecules like ARN have a short half-life. An extended explanation of difficulties of abiogenesis is available at https://www.youtube.com/watch?v=71dqAFUb-v0. This a seriously challenging 12 episodes series about the chemistery required for abiogenesis.
We have been raised by an education system far outdated about the difficulties of abiogenesis (that make appear it so much more possible that is was in reality). This is why no significant success were made since the 60 about this subject.

except self forming nucleic acid chian have been done, it is actually remarkably easy if you not keep purifiying out your samples.https://www.nature.com/articles/nature08013 and  https://pubs.acs.org/doi/10.1021/jacs.0c12955 you may want to update your information A LOT has changed since the 60's

You may want to learn prebiotic chemistry from soneone serious not a creationist shill who openly lies. https://www.youtube.com/watch?v=ghJGnMwRHCs&list=PLybg94GvOJ9HzCxBR9f4oi7MvfVcKAS6O&index=3 as an example  7 years is not a short half-life, it is more than enough time to get billions of reactions, James just lies about the relevent chemistry or worse does not understand it.

The Miller-Urey experiment does not explain the origin of life. It just propose a plausible way to develop life from organic matter, as part of the abiogenesis model of the origin of life. A better approach to understand the theories of life origin is looking for a context.
We already know, by the cellular theory, that cell are the main component of organisms and that just cells could originate others cells. So, the research is focused on finding a way to create at least one cell. From knowed compounds, cells could be modeled as a set of autoregulated biomolecules. Just two of them are used explicitly for replication: nucleic acid and proteins. If you think about this two components, the Miller-Urey experiment just propose a way to develop simple proteins from aminoacids, and aminoacids from inorganic matter. Amazing, but not enough for explaining the complexity of actual proteins and enzymes.
But there are other theories and facts that works well with this experiment. Some non-translated olygopeptides have intracellular functions. The PAHs world theory proposes a way to develop nitrogenated bases from aromatic hydrocarbons. This bases are precursors for RNAs and DNAs. The RNAs world hypothesis establish a way to develop life from RNA and not DNA or proteins. The phospholipid bilayer have some common patterns with micelles and all this mechanisms would be part of the Last Universal Common Ancestor (LUCA). But there is no evidence of the relationships between this theories and maybe there are just too simple for explaining life.
Maybe the first cell had come from the space, where a pre-term version the krebs cycle have been demostrated to work. We could think on it as "biogenesis" until "abiogenesis" could be demonstrated.

"first cell from space" does not solve the problem it just side steps it, also you may be interested is some of the more recent work on RNA synthesis. https://pubmed.ncbi.nlm.nih.gov/33547911/


text:
Vision: what is the difference between on-off ganglion cells and lateral inhibition?
Is 'lateral inhibition' just a term for the biological basis of the functioning of the on-center (or off-center) ganglion cells?
Or do these terms describe separate processes?

Short answer
Retinal center-surround receptive fields are an example of lateral inhibition. It occurs elsewhere in the nervous system too.
Background
Center-surround receptive fields are indeed an example of lateral inhibition, where the ON field suppress the OFF field through lateral inhibition. The center-surround connectivity in the retina (Fig. 1) is indeed the most well-known example of this kind of circuitry. However, lateral inhibition occurs in other sensory systems too, for example auditory and olfactory neurons (Bakshi & Ghosh, 2017). For more information on the retinal circuitry underlying center/surround inhibition see this answer.
References
- Bakshi & Ghosh (2017), Handbook of Neural Computation: 487-513.

Fig. 1. Retinal circuitry underlying On-OFF center-surround conncetivity in ganglion cells. source: New York University


text:
Unsure about definition of "n" and "C" values in mitosis
I am preparing for a Biology exam and I'm reviewing the "n" and "C" notation used in mitosis.
My professor said that when the cell replicates its DNA in S phase of mitosis, we get twice the "amount" (C) of DNA, but we still have the same "number" of chromosomes.
Does this mean that if the replicated chromosomes were to "split apart" from their centromeres, we would have a 4n cell (so a cell with 4 sets of chromosomes)?
At the same time, my intuitive response sort of says, "well, they're replicated, so they're exactly the same, so you'd technically have 2 sets, not 4 right?".

I don’t know what the professor inferred exactly in class. Our somatic cell consists of two set of chromosomes that one set is maternal, and the other is paternal. In other words, human somatic cell has diploid number of chromosomes (2n). However, mature ovum and sperm are haploid number of chromosomes (n). The fertilization combines these two haploids into one diploid.
Somatic cell is always diploid throughout mitosis, but the amount of DNA is duplicated during interphase, especially in S phase. The amount of DNA may be represented as “C” for better understanding. The number of chromosome and the amount of DNA are 2n/2c in G1 phase during interphase. The number of chromosome and the amount of DNA are changed into 2n/4c in S phase. The amount of DNA is separated exactly half into two daughter cells in mitosis. The number of chromosome and the amount of DNA come back to 2n/2c after mitosis.

While I've not heard of the "C" notation previously, "n" is common notation that indicates the ploidy of a cell. The "n" refers to the number of unique chromosomes within a cell. Eukaryotic cells are generally diploid, or 2n. The multiplying number - "2" in the diploid case - refers to the number of versions of each unique chromosome. For example, humans are diploids (2n). We have 23 unique chromosomes (22 regular chromosomes and 1 sex chromosome), but we have 2 variants of each chromosome to give us a total of 2*23 = 46 chromosomes.
Prior to S phase, diploid cells contain 2n content (maybe "content" refers to "C" notation?) of DNA. During S phase the cell duplicates its DNA content generating 2 sets of 2n chromosomes (2 copies of 46 chromosomes for a total of 92 chromosomes in the human case). You are correct in that it is 2 sets of 2n rather than 4n, since the convention would indicate 4n as a tetraploid (many types of plants are in fact tetraploid, https://en.wikipedia.org/wiki/Polyploid).
At the end of the mitotic cell cycle, cell division functions to separate the 2 sets of 2n chromosomes into two distinct cells, each containing 2n chromosomes. If all 4 chromosomes separated from each other and the cell was able to divide into quarters rather than halves, that would yield 4 1n cells. This latter idea is what occurs in meiosis.

For human male, XY are unique chromosomes, that doesn't imply n=24 instead oh 23. Edit your definition please.

I appreciate the point regarding X and Y chromosomes being different relative to each other. They do, however, fall under the same generalized heading of "sex chromosomes", which are a unique subgroup of chromosomes that manifest themselves in different ways in different species (mammalian sex chromosomes versus Drosophila sex chromosomes versus C. elegans sex chromosomes versus ZW system of sex chromosomes). For this reason a more generalized reference to sex chromosomes is appropriate, though I will make edits given the explicit example of humans being used.

See https://en.wikipedia.org/wiki/Sex-determination_system for an overview of sex determination


text:
Can anyone explain the idea of anodic nerve stimulation?
Nerves get stimulated under the cathode, according to the conventional current direction. But in some research, it is said that anodic stimulation or anodic current stimulation can activate neurons. How does it occur physically? The picture below shows the two types of stimulation, but I can't get it.

Short answer
Both anodic and cathodic current pulses can evoke neural activity, as shown in your image.
Background
You have to be aware that the current direction is arbitrary and the 'convention' you mention depends on your discipline. In electrophysiology, the anode is generally considered to be the positive electrode, the cathode is generally the negative electrode and the anode the positive. In physics however, current is assumed to be positive (due to historical reasons) and therefore the definition of anode and cathode is opposite.
Secondly, there is no reason to assume that nerves under the cathode are stimulated (and not under the anode), as is shown in your picture - in both cases a neural response is elicited. For example in cochlear implants, biphasic current pulses are used, because these are safer than simple anodic or cathodic pulses. Biphasic pulses are charge balanced and consist of an anodic phase and an opposite cathodic phase. (Cochlear implants are arrays of electroides implanted in the inner ear that stimulate the auditory nerve directly and are used to treat sensorineural deafness).
In animals and humans, both anodic and cathodic pulses can evoke neural responses. In human cochlear implant users, the anodic phase is more effective than the cathodic phase. In contrast, in animals usually the opposite is observed. The reason for this discrepancy is unclear (Machery & Cazals, 2016).
Whatever the exact reason of their differing effectivity in evoking neural activation - both anodic and cathodic current pulses can evoke neural activity.
Reference
- Machery & Cazals, Adv Exp Med Biol (2016); 894:133-42

In both cases you generate loops of current, with current densities determined by the overall conductive geometry. So a current flowing from the cathode (negative electrode in electrophysiology), and thus imposing negative charges onto the outer surface of an apposed neuronal membrane, would create a local depolarization there, but would also at a distance draw negative charges away from the outer surface of the membrane, albeit with a lower current density, thus creating a local and weaker hyperpolarization there. Now, consider what happens when you switch to an anode. Current flowing from the anode would impose positive charges onto the outer surface of an apposed neuronal membrane, creating a local hyperpolarization there. But it would also draw positive charges away from the outer surface of the membrane at a distance, creating a local and weaker depolarization there. Crank up the current and you can make that depolarization at a distance strong enough to reach threshold. You would thus excite the membrane at that point, despite hyperpolarizing the membrane closer to the anode.
Because the conductive geometry of biological tissue, and thus the current loop pathways, can be quite complex, the effectiveness of cathodal versus anodal stimulation can vary and be hard to predict. Thus, one usually ends up choosing one over the other on purely empirical grounds.

Welcome and thanks for your answer. Answers are required to be backed up by credible sources in this community, preferably journal papers, but credible web pages (hosted by universities etc) are OK too. Wikipedia is tolerated, but I tend to downvote answers based on wiki pages only. I'm bannering this one. Cheers


text:
Is the masking effect of sound related to action potentials or to mechanical aspects of hearing?
I am an applied mathematics / signal processing engineer who wants to learn more and I have a question that has been bugging me for some time. It is known in audio coding circles that human hearing is masked both in the frequency and temporal domain. This means that when two sounds of almost the same frequency are presented, the loudest will overshadow the weakest for short periods of time.
I was thinking that maybe here on Biology.SE I can get some explanation of this phenomenon. Is this masking effect caused by properties of human neurons, or is it mediated by processes earlier than the neurons, i.e.., due to the mechanical aspects of hearing while the sound is entering the ear and hitting the eardrum, or one of the tools behind the drum?

Can you give a little more detail on the type of masking you are referring to? (I ask because in neuroscience all sorts of masks are used which may or may not relate to your thoughts) And, especially coming from a math/signal processing background, what would the masks you are thinking of look like if you put them throw a series of bandpass filters?

I think it is described quite well in the wikipedia https://en.wikipedia.org/wiki/Auditory_masking although I read it first at least 10 years ago in a book on image and audio coding.

I have done some signal processing (10 years or so), so it's mostly the biological aspects I feel that I may be lacking and therefore am curious to learn more about.

Short answer
Both - masking occurs through neural effects, as well as via mechanical effects in the inner ear.
Background
First off, there are basically three types of masking, namely simultaneous, forward and backward masking.
Simultaneous masking experiments are the most basic and likely the most widely used. The most basic type of experiment is listening to tonal stimuli in static (white) noise. In this case, the inner ear is busy processing noise and acoustic probe stimuli (tones) are not perceived by the subject, while loud probe stimuli are noticeable. A more relevant test for everyday functioning is the speech-in-noise test, where speech stimuli are presented in noise. It appears that hearing loss causes folks to have impaired hearing in noise. The amount of impairment in speech understanding in noise exceeds by far the simple decrease in hearing sensitivity. Anyway, I'm drifting off.
Forward masking experiments present a masker before the probe.
Backward masking experiments present the probe before the masker.
To take a step back - the auditory system consists of the peripheral end organ, namely the hair cells in the inner ear (Fig. 1). Those hair cells translate acoustic physical stimuli into electrical currents. These are currents are fed to the spiral ganglion cells in the inner ear. Their axons bundle up in the auditory nerve which innervates the brain stem and ultimately the auditory cortex in the brain.
Now - forward masking experiments are generally regarded to target the peripheral structures, while backward masking experiments target the central structures at a higher level.
Peripheral masking effects occur at the level of

the basilar membrane (e.g. Zwicker (1977)
the auditory nerve (e.g. Stronks et al. (2012)

The basilar membrane is the structure that mediates the (traveling) wave that sounds generate and that traveling wave is the very basis of the frequency analysis in the cochlea, akin to a place-dependent Fourier transform. It is the basilar membrane that separates frequencies from high at the base to low frequencies in the apex due to its physical properties. Now, when the basilar membrane is busy moving in response to a masker presented at 1 kHz at 100 dB SPL, a probe tone of 1 kHz presented at hearing threshold (0 dB HL) will be totally swamped, simply because the amplitude of basilar membrane movement will be changed by next to nothing.
The auditory nerve is also an important neural site where masking occurs (e.g., Stronks (2010). This has to do with the fact that neurons fire action potentials. After a neuron has fired an action potential, there is an absolute refractory period that takes several ms to resolve. In that time, ion channels previously engaged in firing are re-opened and up and ready for the next action potential. Within the absolute refractory period, no stimulus, whatever its strength, can evoke another response in that neuron. Following that, a relative refractory period follows in which its firing threshold is increased, but strong enough stimuli can evoke a response. If a neuron is busy firing after chronic stimulation, it gets tired and a state of adaptation follows. Further stimulation results in fatigue, in which the neuron gets tired and has exhausted its resources to fire. All these processes can result in masking of simultaneously presented stimuli (simultaneous masking), but notably also in stimuli presented after the masker has subsided (forward masking).
Now, all these processes will not affect backward masking, where a short probe stimulus is swamped by a following masker (e.g., Oxenham & Moore (1995). This is caused by more central, higher-level processes that include attention processes, i.e.,

the brain

In other words, the following masker distracts the attention of the subject that in turn fails to notice the probe. It's thought to depend on central processes as peripheral processes can't be 'fooled' and faithfully transmit the stimulus to the brain, whatever comes next.

Fig. 1. The inner ear (cochlea) features hair cells that are actiovated by sound waves traveling through the basilar membrane. source: Modesto Junior College
References
- Oxenham & Moore, JASA (1995): 98; 1921
- Stronks, PhD thesis, 2010, University of Utrecht
- Stronks et al., Otol Neurotol (2012); 33: 35-42
- Zwicker, JASA (1977); 61: 1031

This is a very good and thorough answer! I would upvote more if I could.

@vkehayas Yep I would like to do that and award the answer retroactively, but my credits are low on my biology account so I will probably crawl under limits for commenting if I do. Unless it is somehow possible to transfer some of my math.SE points to award the answer.

It is definitely an outstanding answer which deserves bounty and praise and honey in the coffee. I was thinking I should wait a bit more to give others a chance too, as I know how frustrating it can be if an answer is accepted right away if I am in the middle of writing one myself.


text:
Unlike humans, why do plants not have something blood-like to transport $O_2$ throughout their body?
Since plants have a large number of stomata at different parts of their body, they can get $O_2$ at almost every part of the plant and so, they don't need to transport it throughout the whole body whereas in the case of human beings, they can only intake $O_2$ through their nostrils, but a large number of organs throughout their body require it. So it needs to be transported. And for this reason, blood is present.
Let me know if I'm wrong and what the actual answer is.

In plant cells, O2 enters through stomata or lenticels. Then, the O2 molecules are transported to the cells through the process of diffusion. Stomata and lenticels are found all over the surface of plant body, i.e., leaves, stem and root. Because of this, plants don't need blood like connective tissue to transport O2 and CO2.


text:
Aging and death of perennials
Perennial plants species generate a new plant annually from the same parent root stock. At the end of the year that new shoot withers and dies, to re-appear the next year. Hence, the above-ground parts of perennials obviously age and die, but what about the rootstocks?
Are the rootstocks from perennial plant species immortal, or do these rootstocks age and die as well?

http://biology.stackexchange.com/questions/13777/cell-life-division-for-immortality-or-reproduction-with-aging/13809#13809 answers the uniucellular question accurately and see Remi's suggestions. I edited the question to leave the rootstock part. That seems to be a valid new question.

Note that you describe herbaceous perennials, as not all perennials die back each year (e.g., evergreen perennials and woody plants like trees and shrubs retain their shoots).

I have a number of rose varieties that have been propagated from cuttings & divisions of plants bred in the 1800s.  And there's an aspen clone said to be about 80,000 years old: https://en.wikipedia.org/wiki/Pando_(tree)

The issue is based on your perception of what an individual ought to be. The concept of individual is actually often hard to apply in biology and therefore is the concept of ageing. In other words, the wish to categorize is a rather human tendency but it may fail to make objective representation of biodiversity. The book The Major Transitions in Evolution Revisited makes a very good job to explain the difficulties to deal with the concept of individual in biology.
You seem to be happy to consider an offspring be a different individual if you can still perceive the parent individual. In bacteria, both resulting cells could be considered as offspring and therefore new individuals. Note however, that asymmetrical division bring some more blur into these categorizations.
Note also that single cell bacteria do age. See the wikipedia article on bacterial ageing. You might also want to have a look at the wikipedia article on biological immortality as well as the posts Why is the Hydra Biologically Immortal? and Do crocodiles age?.

I edited the question - see my comments. Please feel free to revert those changes, but I think the unicellular part is duplicate. Perhaps you can add a sentence on perennials? Up to you.


text:
Why can't we kill ourselves by holding our breath?

Is it possible to kill yourself by holding your breath?

This question is obviously copied from Quora, but I had heard it as a fact that we cannot kill ourselves by holding our breath and I'm looking for a referenced answer.

NAA, since it relies on something other than breath-holding.. but you could kill yourself if you do the over-pressure+hold breath trick to make yourself pass out and happen to hit your head badly when you land.

Or fall into water face-down, for a less gruesome death.

How do you know that we can't?

@SEwontLetMeDeleteProfile Because, even if we do it long enough to pass out (which is difficult except for under specific circumstances), we will immediately start breathing again.

The question "why" is ambiguous. Answer "because we evolved this way" is equally good but likely not what you're looking for.

Short answer
Healthy people cannot hold their breaths until unconsciousness sets in, let alone commit suicide.
Background
According to Parkes (2005), a normal person cannot even hold their breath to unconsciousness, let alone death. Parkes says:

Breath‐holding is a voluntary act, but normal subjects appear unable
  to breath‐hold to unconsciousness. A powerful involuntary mechanism
  normally overrides voluntary breath‐holding and causes the breath that
  defines the breakpoint.

Parkes explains that voluntary breath‐holding does not stop the central respiratory rhythm. Instead, breath holding merely suppresses its expression by voluntarily holding the chest at a certain volume. At the time of writing, no simple explanation for the break point existed. It is known to be caused by partial pressures of blood gases activating the carotid arterial chemoreceptors. They are peripheral sensory neurons that detect changes in chemical concentrations, including low oxygen (hypoxia) and high carbon dioxide (hypercapnia). Both hypoxia and hypercapnia are signs of breath holding and both are detected by the chemoreceptors. These receptors send nerve signals to the vasomotor center of the medulla which eventually overrides the conscious breath holding.
The breaking point can be postponed by large lung inflations, hyperoxia and hypocapnia, and it is shortened by increased metabolic rates.
Reference
- Parkes, Exp Physiol (2006); 91(1): 1-15

In addition: even IF you could hold your breath 'till unconsciousness, because it's a conscious act you'd start breathing again as soon as you're out.

My understanding (from dim-and-distant Chemistry O-Level days) was that it's primarily the build-up of carbon dioxide that prevents you holding your breath long-enough to pass-out/die... breathing into a bag containing a CO2 adsorber would/may allow this to happen.

@TripeHound Hyperventilating, to reduce CO2 build up, is one of the main causes of Shallow Drowning - it not only can, but does happen.

How universal is this?  I've heard various times that young children will use breath-holding as a coercive tactic against parents, and the best way to deal with it is to just let them keep at it until they pass out, at which point they involuntarily start breathing again, and they'll very quickly learn not to do it anymore.

@MasonWheeler I've heard similar stories, but couldn't find peer reviewed work on it; my answer is based on a sound paper in a credible journal, at least afaik

"Healthy people cannot hold their breaths until unconsciousness..." I've seen this done.

Which brings us to "Always listen to experts. They'll tell you what can't be done, and why. Then do it." --- Lazarus Long

Although - note that Parkes doesn't say this can't be done, but that it wasn't observed while attempting it, and that it appears it can't be done.

Does this mean that when people who are trapped underwater drown that they were conscious when they drowned. Even if they attempted to hold their breath that they had no choice but to breath in water. What a horrible thought as I knew a person who drowned after getting caught up in weeds.

@cgTag Yes, if they didn't hyperventilate or have some other health issue. Though note that you only really breathe in a small amount of water - the trachea gets sealed on contact with water - and this phase usually only lasts for a few seconds before unconsciousness sets in (the reflexive breath triggers only a short while before cerebral hypoxia in most people). There's still some time to save the victim afterwards - near drowning isn't rare. There's even some extreme cases in cold water where people survived the anoxia for minutes without any permanent damage (even 60 minutes!).

Counterexample: At least some people can train themselves to hold their breath until they pass out, and if this occurs underwater they will almost certainly die by drowning.
When I was in military service I became friends with some U.S. Navy SEALs.  They go through a notoriously difficult training and selection process (BUDS) that has been well documented.  Among the program's "evolutions" are tests in which candidates have to solve problems to access SCUBA units while submerged in pools or water tanks (and while being harassed by instructors).  It is common for candidates to pass out during these tests, because if they surface for air they fail the test.  (And these are people who self-select as very motivated to not fail at any cost.)  Apparently the tests weed out candidates who are prone to panic as they lose oxygen and can't override their physiological instinct to breath.
I spoke to one graduate who passed out during one such evolution (but succeeded on a second attempt).  He noted that after that incident he lost any fear of drowning, because he realized that if he ever found himself in a situation where he was running out of oxygen he would not feel panic and would just fall unconscious before drowning.

@Trilarion: Yep, just added link to news report on the subject.  Notable quote from that article: “What you’re seeing in the data is more rigorous documentation,” Davids said, suggesting that five students losing consciousness in four months wasn't unusual at BUD/S.

A similar effect (Wikipedia, check the references) is why swimming pools often ban distance swimming underwater: hyperventilation reduces CO2 in the body, even to the point where lack of oxygen causes blacking out first, but more often enough that the swimmer doesn't have time to surface after the urge for air becomes strong. If  the SEALs are hyperventilating first, and determined to stay under, no wonder they're passing out.

I'd expect that training could make this more achievable. Even so, when I witnessed this done it was a female classmate in 6th grade. It's at least possible for the untrained.

Hyperventilation is a special case: The urge to breathe is not triggered by lack of blood oxygen, but by excess of blood CO2. Hyperventilating substantially decreases your blood CO2, but only marginally increases your blood O2. In other words, it delays your urge to breathe without significantly delaying your need to breathe.

This counterexample does not support an ability kill yourself by holding your breath. You pass out, then something happens because you aren't conscious (you drown, under water). The same thing would happen if you held your breath until you passed out while driving, balancing on a tightrope without a net, sitting in a burning building, skydiving before pulling the ripcord, or running from a murderer. In all of these situations the official cause of death would not be holding your breath.


text:
Are genes uniformly dispersed throughout the genome?
I think that telomeres and centromeres are regions with a very low gene content (= regions that contain few genes). To the exception of telomeres and centromeres, are genes uniformly distributed throughout the genome or do they tend to clump together or to scatter as much as they can? Do genes tend to clumped or avoid specific regions such as regions with low mutation rate or low recombination rate?

No they are not. High gene density is correlated with GC content. Most genes are found in GC rich isochores, which are not distributed uniformly (as can be seen on any karyotype). It is also shown through direct sequence analysis (gene density shown in red, GC content in green):

Venter et al. go on to say:

This inhomogeneity, the net result of millions of years of mammalian gene duplication, has been described as the “desertification” of the vertebrate genome. Why are there clustered regions of high and low gene density, and are these accidents of history or driven by selection and evolution?

Desertification refers to this 1985 article by Ohno:

The net consequence of hundreds of millions of years of continuous gene duplication is the desertification of the euchromatic region of modern vertebrates; the average distance between still functioning gene loci becoming progressively longer.

This would seem to suggest that these deserts are the result of gene duplication and subsequent degeneration into pseudogenes, though this is surely not the only cause. I'm not sure that your last question or those posed by Venter et al. have an answer as of yet. This more recent paper offers some interesting ideas (references removed for brevity):

More than 20 years ago, Ohno (1985) postulated the desertification of the euchromatic region of the higher vertebrates’ genomes owing to continuous gene duplication events followed by degeneration of newly emerged gene copies in their evolutionary history. Only with the first release of the complete sequence of the human genome in 2001 was Ohno’s prediction of the existence of such deserts confirmed. Another mechanism to generate imbalance of gene deserts between chromosomes might be large intra-chromosomal duplications, from which some mammalian-specific gene deserts appear to have evolved. However, the functional or evolutionary significance of gene deserts is not yet fully understood. At first glance, gene deserts seem to be devoid of biologic functions because of their lack of protein-coding DNA. Despite this, some gene deserts have been shown to contain important regulatory and sometimes ultraconserved regions for neighboring genes that function over large distances. In addition, the observation of stable gene deserts with homologous flanking genes (often transcription factors), which are maintained for long evolutionary durations, as well as the existence of numerous conserved nongenic sequences in mammalian genomes suggest that gene deserts are not just genomic junkyards but instead might be of functional significance. However, some gene deserts can be deleted without noticeable phenotypic effects. Thus, it remains unclear whether the uneven accumulation of gene deserts in eutherian chromosomes, which appears to be the strongest causal agent for the observed relative lack of a NG/LC relation in the genomes of placental mammals, is simply a byproduct of their genome evolution and possibly the long-term decrease in population-size, as would be suggested by the enrichment of gene deserts along the evolutionary lineage leading to mammals. Upcoming detailed reconstructions of ancestral vertebrate genomes will help clarify these points.
Alternatively, this particular architectural feature of eutherian genomes might be linked to some of their morphologic, physiologic, neurologic, and cognitive evolutionary innovations, possibly by regulating genes with essential functions in development. It has recently been hypothesized that regulatory elements in gene deserts function in the regulation of core vertebrate genes. Furthermore, approximately 20% of conserved noncoding elements are eutherian-specific. Thus, the uneven distribution of gene deserts could itself be caused by an underlying pattern of uneven distribution of some core genes in placental genomes. This hypothesis should be tested in the future.


text:
Na+ / K+ ATPase: How does it restore resting membrane potential?
Could not find any sources talking about this (in a clear manner). If the Na+ / K+ ATPase pumps 3 Na+ out for every 2 K+ it pumps in, thus making the cell more negative, why is the Na+ / K+ ATPase used to restore resting membrane potential following hyperpolarization? Wouldn't that must make the cell more negative, which is the opposite of what we want?

The Na+ / K+ ATPase is not "used to restore resting membrane potential following hyperpolarization", it is used to maintain the concentration gradient of sodium and potassium.

@BryanKrause: How are the concentrations of Na+ and K+ outside / inside the cell rebalanced after hyperpolarization then?

Try also https://biology.stackexchange.com/questions/76166/ambiguity-about-the-relation-between-membrane-potential-and-concentration-gradie/76167#76167 https://biology.stackexchange.com/questions/57064/why-is-it-possible-to-calculate-the-equilibrium-potential-of-an-ion-using-the-ne/57066#57066 https://biology.stackexchange.com/questions/66166/are-cells-electrically-neutral-or-charged-to-setup-the-membrane-potential-across/66174#66174 in addition to the marked duplicate https://biology.stackexchange.com/questions/77919/why-does-resting-potential-not-become-continually-more-negative

The sodium-potassium pump does keep the concentrations of Na+ and K+ constant in the long term, but that's not necessary for transient changes like you get from receptor activation or action potentials, those are governed by opening and closing of passive ion channels.


text:
Role of the pupil response in night vision
What are the things that affect the reaction time of pupil light reflex? What I mean to say is, if you are in a bright room, and the light suddenly turns off. The time you spend to see things in the room (i.e.., night vision) is the reaction time.

pupil dilation and contraction (the pupil light reflex) and retinal production for night vision (a it room suddenly going dark) are very different things, which are you asking about?

Short answer
Pupil responses have little effect on dark adaptation. It is the retinal processes that govern the bulk of the dynamic range of the eye's light sensitivity.
Background
You are referring to dark adaptation of the eye, which is, according to the Universty of Calgary:

This change is called dark adaptation and refers to the process by which the eye becomes more sensitive to light under conditions of reduced illumination. [C]ones are primarily responsible for resolving fine detail (acuity) and colour vision in good light, while rods allow us to see more effectively in dim lighting conditions. The recovery of sensitivity in dark adaptation involves the regeneration of photoreceptor photo-pigments as well as neural changes.

See figure 1. The rods are way faster in gaining sensitivity than the photon-hungry cones.
In a typical clinical setting for diagnostical purposes of e.g. rod function, a typical dark adaptation period is about 20 minutes or so, which fits the below graph quite well. At the end of dark adaptation, the eye is about 100,000 times (i.e., 5 log units) more sensitive than it was at the beginning of the test, a level called dark adapted sensitivity (Universty of Calgary).
In contrast, the pupil response has only a minor effect on light sensitivity in  dark adaptation. It does change its diameter in the dark for sure, but the amount of light that passes through doesn't change too drastically. Pupil diameters range between about 2 and 8 mm (Spector, 1990), say a factor of four. In terms of surface we are talking about 3 and 50 mm2, respectively using (pi*r2), hence a factor of 16, as opposed to 5 orders of magnitude in the process of retinal adaptation.

Fig. 1. Light sensitivity adaptation of rods and cones. source: Uni Calgary
Reference
- Spector. The Pupils. In: Walker et al. (eds.) Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd ed. Boston: Butterworths (1990)


text:
PCR related problem
Recently, I have done a PCR of a region of human p53 gene and got faint band after that. Then I used that PCR product as input and did a nested PCR with same PCR condition, but now the specific band disappeared and only smear was there. Can anybody help me to solve the problem. Why that happened and what should I do to get specific band.

Can you tell us what the template DNA was in the first PCR?

More detail of both protocols would be helpful.

Ther could be different problems affecting your r salts. Maybe the primers you are using are not specific enough or your PCR condition are not optimal. I would first check the primers by blasting them against the human genome to spot mismatches. If your primers do not bind uniquely to your gene of interest then design a new pair. If the primers are ok, then I suggest you to run a grandient PCR (annealing temperature from 50 to 65 degree Celsius) to determine the optimal annealing temperature of your primers. These two steps usually solve 99% of my PCR problems, assuming that your template DNA is ok and at the right concentration. If even with the gradient PCR you can't find a good condition, the next step is to play with the buffer by changing magnesium chloride concentration and maybe adding betaine.


text:
How to calculate Fst from AMOVA
I calculated an AMOVA from a genind object, with one hierarchical factor. In the table I obtain there are SSD values (for my grouping factor,"Error" and total) and sigma2 values (for my grouping factor and "Error")
I have two questions:

What does "error" stand for?
How do I calculate Fst? Which values do I have to use?

Welcome to Biology.SE. It may help if you could include the AMOVA outputs (or some of the outputs). Also, what software did you use to calculate your AMOVA?

I have never performed an AMOVA myself and I don't know what a genind object is. But ...
Error
Typically, "error" can also be called "residuals". In other words, it is the sum of squared deviation between the data and the regression line (just like in any regression model). You might want to learn a little bit about regression and ANOVA to understand your AMOVA.
Fst definition
From Nei 1973 (very good paper, I recommend reading it),
$$F_{ST} = \frac{H_S-H_T}{H_T}$$
, where $H_S$ is the average subpopulation variance in allele frequency and $H_T$ is the total variance in allele frequency.
What you probably got from the AMOVA output
You should have these info in your AMOVA output. If it only give you the total variance and the between group variance (which is what is used for the F-test), then just remember that the among variance is the total variance minus the between group variance.

Thanks for your input! I found out that Fst cannot actually be calculated from the AMOVA, since I am not given the total variance in allele frequency. As to the error, in the AMOVA it refers to the variance which cannot be explained by the grouping factors I have fixed.
A genind object is an object used by the library adegenet on R, which contains allelic information about a group of individuals. It enables you to carry out many types of analyses such as multivariate analyses. Sorry for not specifying it in my post!

The AMOVA output probably gives you at least 2 of the following 3 statistics: Total variance, between group variance, within group variance. If you have two of them, you have the third one. Yes, exact you got it for the "error" term. As said, you might want to reinforce your understanding of simple ANOVA. Here and here are short videos that may help you.


text:
Where does the mass come from when you grow plants in water?
How do plants like green onions seem to grow forever when put in jar of water?  I understand that plants get a lot of their carbon from the air (as per this question) but surely they need more than just carbon to grow new leaves.
The answer in the linked question mentions that plants in general get their mass from sources like water and nutrients like nitrogen and phosphorous, and ions.
However, if a plant is growing directly in [distilled] water where will it get those nutrients (like phosphorous and the ions) from?
Where does that extra mass come from?

Right there in the first answer to the question you linked to is a statement that shows that over half the mass added by the plant comes from a particular source other than air.

The sources it mentions are water and then specific nutrients like nitrogen and phosphorous, and ions. However, other than the water where do those other items come from

If you put the onion in distilled water only, the plant will not get any more nitrogen, phosphorous, or ions. The onion has some stores of these atoms, though, and will continue growing a good while since the bulk of needed molecules (cellulose, sugars) are formed only from carbon dioxide and water.

Short answer
Plants with storage compartments can grow for extended periods on water alone.
Background
It indeed seems the question is indeed different from the suspected dupe after all.
According to Turesson (2014)

Seeds, tubers and roots are the most common sites for [...] energy storage and the forms in which energy is stored are predominantly oil, starch and sugars. Underground storage organs mainly store starch and sugars, while seeds from different plant varieties accumulate high levels of starch and also oils and proteins.

So storage compounds like "seeds, tubers and roots" can sustain prolonged growth in the absence of pretty much anything, except water; just consider the familiar seedlings of cress on cotton wool (Fig. 1). There's basically nothing there, just water.

Fig. 1. Cress grown on cotton wool and water. source:Dreamstime
Reference
- Turesson,  Carbon Allocation in Underground Storage Organs, Doctoral Doctoral Thesis (2014), Swedish University of Agricultural Sciences
Alnarp

The most common elements in organic chemistry are carbon, hydrogen, oxygen, nitrogen, sulfur, and phosphorus.
Water provides hydrogen and oxygen; air (on Earth) provides oxygen, carbon (mostly CO2), and nitrogen. This leaves out only sulfur and phosphorus.
Therefore, any plant that needs only trace amounts of sulfur and phosphorus (or already comes with all that it needs) could grow reasonably on air, water, and light. Bear in mind that another limiting factor is trace amounts of magnesium in chlorophyll which can't be replenished on air and water.

I'm failing to see how this answers the question. Further, an answer needs to be backed up by sources.


text:
Where can I find resources of the biological processes occurring after death of a mammal at various temperatures?
Using google I usually end with results in cell death. I found some layman articles, but that does not help.
My main interest is the brain part.

I believe William Bass has written on this, probably in the Journal of Forensic Sciences, but no specific articles come to mind. I'd start by looking for his articles, then probably with a variety of search terms using a filter for that journal. It's not open access, so you'll need to use a library or institution that has a subscription.


text:
External "lungs" that process your blood the same as your real lungs do - would that stop your need for breathing?
So say your blood goes with a tube out of your body. In an external device all the chemical/biological magic would happen and it would be fed back to your body.
Of course this doesn't exist (yet), but if this would be possible - would it mean you automatically stop your need for breathing?
Is "gasping for air" linked to the amount of oxygen in your blood? Or is there something else going on?
Just a random (theoretical) shower thought. The idea that you wouldn't feel the need to breath feels weird to me.

A device that fits your description does seem to exist, namely an ECMO machine that delivers extracorporeal membrane oxygenation (Fig.1 ). It is defined as:

[A] machine [that] pumps blood from the patient’s body to an artificial lung (oxygenator) that adds oxygen to it and removes
carbon dioxide. Thus, it replaces the function of the person’s own
lungs. The ECMO machine then sends the blood back to the patient
via a pump with the same force as the heart, replacing its function.

The response of patients to ECMO appears to be variable (Crotti et al., 2017):

As the physiologic cardiorespiratory variability is increased in this condition, the dynamic interaction between patient respiratory activity and extracorporeal system function affects the clinical management. The effect of extracorporeal CO2 removal on patient respiratory drive is variable and not always predictable, with some patients responding to CO2 removal with a decrease in respiratory rate and effort and other patients demonstrating a persistently high work of breathing independent on CO2 unload.

Breathing and undoubtedly the exaggerated gasping for air after heave exercise is related to the concentration of CO2 in the blood that's monitored by the brain. Those chemoreceptors basically measure the pH of the blood. However, pulmonary pH receptors exist and a multitude of other physiological mechanisms are at play to keep the level of O2 in check . I happily refer to Brinkman et al. (2020) for an overview on O2 and CO2 homeostasis.

Fig.1. ECMO. source: University of Iowa
References
- Brinkman et al., StatPearl
- Crotti et al., J Thorac Dis. 2018 Mar; 10(Suppl 5): S661–S669