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What's this mold? (With microscopic images)
So I (living in NRW, Germany) found an apparently quite homogenous mold colony at home, and would like to know what type of mold it is.
How I found the colony, where it grew:

I ate something, then took a little nap, then woke up later a little nauseous. I blamed it on the food (which still is a plausible possibility).
Then I noticed that my room smelled a little different from the stairwell (a little sour), and went searching for rotten stuff.
I then found a large bowl with a little food leftovers and a huge mold colony.
I remembered that some days prior, I removed a plate with food leftovers that was stacked on top that bowl, ironically because it had gotten moldy (with what looked like a different type of mold).
Given that there was lots of mold in the bowl and I had removed the plate only some days prior if I remember correctly, the mold probably already grew in the bowl with the plate stacked on top, shielding it from light, and severely limiting air exchange, until I removed the plate, of course.

I made several images of the mold, one of the colony, which had grown on two leftover noodles, and several of the mold's structure, including its fruitbodies, under the microscope. All but the last two microscopic shots were made with the light coming from below, the last two shots were made with the light coming from above, if I remember correctly.
The images:
Image 1:

Image 2:

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I'm no expert, but there's a key here - it has picture and text keys in links inside the page. I think possibly Rhizopus or Mucor.

Thanks for pointing me to the "key", I didn't know such things existed.
With the help of the key, I now managed to form my own hypothesis of what fungus this is, tough I won't mention it to see if others independently arrive at the same answer, to check its "plausibility".

Keys of this sort have existed for a long time - I think it was around the 1700's they were invented. Certainly Lamark used them, but I think they were around before him.


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Is it possible to plant tardigrade DNA into a human? What would happen even if?
So I have been reading a WEBTOON (A distant sky) and the 2 mcs have tardigrade stem cells in them which gives them the abilities tardigrades have. I am aware that the story is obviously fictional, but I was wondering if it is possible? What would happen?

Welcome Pluto. Could you read the [ask] section of the [help] and [edit] to include more (much much more) specific details of what you're referring to in terms of the specific "genes", where and in what cells you'd transplant the "genes" and in what position on which chromosomes, and your own research into the topic. You could do worse than start with this paper: Extremotolerant tardigrade genome and improved radiotolerance of human cultured cells by tardigrade-unique protein

This is like asking what would happen if you put helicopter parts into a bicycle.

Well thank you Jim for answering properly unlike some

These are comments not answers. You're still expected to edit the question to show your own research as per the [ask].

Yes, parts of tardigrade DNA that code for specific proteins or abilities could potentially be isolated and inserted into human cells in vitro. Getting them into a living human is technically possible, but nothing like that has been done. This doesn't mean the process would result in any tardigrade-like effects in the human cells.
However, tardigrade survival is a complex system, not a single superpower gene. You can't just insert 'the tardigrade gene'. Multiple systems would need to be altered successfully for anything close to tardigrade-like resilience. Even if a tardigrade protein was successfully integrated into a human cell, we don't know what would happen because that protein will interact with the rest of our human biology.
As the comments indicate, this is entirely dependent on the specific gene you insert. There are many genes, and each can have a different effect. Many genes also need other systems or other genes to function properly. Also, inserting tardigrade stem cells into the body is different from inserting genes into human cells.

source: Stack Exchange

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

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What's pooling in the spread plate technique?
"Distributing the organisms by rotating the spreader rather than the plate tends to cause more pooling of the inoculum."
https://asm.org/ASM/media/Protocol-Images/Preparing-Spread-Plates-Protocols.pdf?ext=.pdf

Forming a pool (second definition in link); forming a small amount of liquid on a surface. A la "I knocked my cup over and the coffee formed a small pool on my bench"
Basically this results in a concentration of the organisms in one area, rather than an evenly distributed spread.

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


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Are these objects we found ambergris? How to distinguish ambergris from other deposits/minerals
These two objects below were found on the East Coast of the North Island of New Zealand on seperate occasions but within 5km of each other.
They both had a strong and unique, neither pleasant nor displeasing scent to them which has since faded.
The larger of the two is slowly shedding/crumbling small white clumps, presumably as it continues to dry up, a little lump of a resin like material has also become dislodged. The smaller of the larger two lumps has stayed fully intact.
Are they ambergris?
How can an amateur determine if they are or not? What else could they be?

This is unlikely to be ambergris. As I understand it, ambergris tends to darken with age and be a waxy substance with a low (~60 C/140 F) melting temperature. and should melt a little in your hands to give a waxy feel. The smell should be animal- or fecal-like.
Your last image shows a crystalline substance with obvious fracture planes, which means that it is some sort of solid.
I think this is almost certainly the resin from a species of coniferous tree. As you are on the East Coast of the North Island, it could well be pieces of *Agathis australis (Kauri) gum/resin, especially so if you are in Northland or the Coromandel. Kauri are only found about as far south as the bottom of the Coromandel/Kaimai range in the East and down to around Kawhia in the West.
If it is Kauri gum, it will be hard and have a pinetree-like scent, especially when scratched. You should also be able to polish it with turpentine. Kauri gum is semi-fossilized and a form of amber.
Auckland Museum has some pieces of Kauri gum that resemble what you have, and you can find this image on Wikimedia Commons:

Auckland Museum, CC BY 4.0 https://creativecommons.org/licenses/by/4.0, via Wikimedia Commons
Or this one from Te Ara (The Encyclopedia of New Zealand):

Interesting, I shall gently warm some up and see what happens

I don't have very good temperature control, but it does melt under a heated knife. However I read that kauri gum also readily melts ¯\(ツ)/¯


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Formation of xylem
Does metaxylem forms from protoxylem?  Or they develop independently? My main motif is to clarify, " Is metaxylem just a more developed protoxylem? "


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Why doesn't the brain filter out tinnitus noise?
Human sense receptors quickly become insensitive to constant stimulation and even the human brain can effectively filter out and ignore constant stimuli. For example, people living by a busy road soon ignore the noise of traffic and even sirens are hardly noticed. I used to live close to a highway, but never noticed the noise, except for the occasional exceptionally noisy truck or motorbike, even though the actual traffic noise was constantly changing.  Why is it that people who suffer from tinnitus cannot do this?

Remember the need for showing your own research when posting a question. Perhaps look into the basis for tinnitus itself. The Wikipedia article seems to be a good starting place.

I think this question is the same as "what is the mechanism of tinnitus?" or similar; otherwise it's a bit tautological. Like any disease or disorder, tinnitus is what happens when the brain "creates noise" instead of filtering it out. There's no real sound in tinnitus, unlike the highway example.

"Why is it that people who suffer from tinnitus cannot do this?" Why do you think they can't? I've had tinnitus for about 50 years. While it was quite noticeable initially, I hardly ever notice it now. It's not that it's gone at times; it's always there. It just doesn't register most of the time.

@BryanKrause - That doesn't mean it never gets "tuned out". I know it's very distressing to some people (it must be worse than mine.) But I definitely tune it out; sometimes even if there's dead silence, it doesn't register unless I think about it.

@anongoodnurse Sure, but the symptom of tinnitus is specifically the experienced sound. If you're tuning it out and not hearing it, your tinnitus is by definition reduced or absent.

The link to the previous question does state that when the initial event is not traumatic people do experience spontaneous habituation. So this does answer my question.

@BryanKrause - I'm not sure I agree. The sound is always there. People can get used to a lot of things if they've had it for almost 50 years. I know the difference between fluctuating tinnitus (how it presented initially) and what I have now. It's not a case of now it's here, now it's not.

@BryanKrause - In one of the links in the previous answer, there is a mention of habituation, but it also stated that if someone has had tinnitus for more than 2 years, it's probably permanent. I wasn't able to tune it out initially for, I'd guess, a decade. I distinctly remember my surprise the first few times I realized i had tuned it out.


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What is this arthropod? (found in Lapland - Finland)
I found this arthropod climbing the wall of my room in Lapland, Finland.

(the max width is about 0.5 cm)
What is it? Is it dangerous?

The picture is not great but I'd assume a pseudoscorpion of some sort. Here is one common species found where humans live but I can't be sure about Lapland specifically and doubt ID is possible at the species level from your image: https://en.m.wikipedia.org/wiki/Chelifer_cancroides
If so, I'm not aware of any harm from these directly, but they can be predators of insects that eat rotting wood, which in turn may indicate a problem with moisture in your structure. A single sighting is not something I would worry about unless you have other signs from those sorts of prey themselves.

thank you the image in the wikipedia link you shared matches

According to this observations map, pseudoscorpions do live in Lapland, as does C. cancroides specifically.


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T-tubules in Muscle Cells
I understand that T-tubules are common to striated muscles such as skeletal and cardiac muscles (with smooth muscle cells having caveolae) but what precisely (if any) is the difference in the T-tubular systems of skeletal and cardiac muscle cells?

The Wikipedia article T-tubule describes the differences.


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Other than the major histocompatibility complexes, what is the difference between professional and non-professional antigen presenting cells?
Can both professional and nonprofessional APCs activate helper T-cells? Or is that only macrophages and B-cells?
Do cytotoxic T-cells only make non-professional APCs go into apoptosis?


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What is the biological pathway for the biodegradation of DDT (pesticide)?
There are various micro organisms which can degrade DDT. Which micro organism is most frequently used for biodegradation of DDT and what is the metabolic pathway by which DDT is degraded?


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Griffith's Experiment Conclusions
My teacher gave us these two questions on Griffith's experiment.

How did Griffith's experiment rule out that the rough cells could have used the capsules of the smooth cells to become pathogenic?

Why did Griffith know this experiment was important?

They said the answers were that

If they incorporated the broken capsule, then the next generation will not have the capsule, that's why we know it wasn't the capsules that made the rough cells pathogenic.

It ruled out proteins were the genetic material.

My problem with these answers is that it relies on knowledge we know. For the answer to number 1, the capsule could have contained genetic material and passed it on to the daughter cells (we know that isn't true but they didn't know proteins weren't the genetic material back then). I don't think the experiment ruled out the capsules were the factor making them pathogenic at all. I feel like all the experiment proved was that bacteria could transform. Beyond that, from my understanding, it didn't prove nor rule out what was leading it to transform - whether it was through protein or DNA.
What am I missing here? If my teacher is incorrect, what should I put down?


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Does decompression sickness (the bends) ultimately come from the change in pressure in the lungs, or the actual total ambient pressure over the body?
I am not well versed in physiology, and I've found the literature available to me confusing on this point.
Mostly I'm going off of wikipedia, mind you. The article on Decompression Sickness' Mechanism Heading states:

Under normal conditions, most offgassing occurs by gas exchange in the
lungs.[53][54] If inert gas comes out of solution too quickly to allow
outgassing in the lungs then bubbles may form in the blood or within
the solid tissues of the body.

What I can't figure out is if the actual ambient pressure matters, if we suppose that that is separate from the pressure in the lungs. From what I've understood, in SCUBA diving the water pressure applies pressure to the air you're breathing (somehow? through the air hose? I'm not certain my understanding is correct) and thus the air you're breathing and the air in your lungs is also at a higher pressure. If I'm wrong about that, that may be the ultimate answer of my question.
I'd like to present a hypothetical, to clarify the exact focus of my question:
Let's say we can somehow form a perfect airtight seal around the waist of an otherwise naked human being. Setting aside the practicality of that, of course. The point is that the human is otherwise unaffected, but it blocks air.
That air tight seal around the person's waist makes it so that their lower body and legs are exposed to a very low pressure environment, maybe even pure vacuum. The person's upper body (and notably their nose and lungs) are in a standard sea-level terrestrial atmosphere.
Putting aside the vacuum bruising and painful swelling and other detriments caused by the low pressure environment on their lower body, my question is this: could the person in this hypothetical get the bends, simply because of the lower pressure on part of their flesh? Or would decompression sickness not be an issue because their lungs are pressurized?

Your scenario is impossible because of blood vessels. If you cut the lower half of the body away while sealing it, and reduced the pressure dramatically, yes, bubbles would form in the now non-functional blood vessels.

@anongoodnurse I don't understand. I'm not implying that the seal cuts physically through the body, just around it but forms a tight seal with the skin.

I understand that. But I'm saying because blood vessles keep ferrying blood to and from the lower body, your thought experiment is impossible to carry out.

If you did carry it out you wouldn't get bruising in the lower limbs, you would extrude everything in the upper body through and into the lower body. It would get very traumatic and gory very quickly.

Ah. I was under the impression that connective tissue is rigid enough to compensate for that, and that the heart would be doing its best to maintain blood pressure for at least a short time. Obviously swelling and bruising would occur, but I wasn't sure that it would necessarily follow that nitrogen would emerge from solution as in the bends.

The solubility of a gas in a liquid is proportional to the partial pressure of the gas above the surface of the liquid Henry’s Law (On the ground at sea level air pressure is about 15psi, nitrogen is about 80% of air, so the partial pressure of nitrogen then is about 12psi.)
When a diver is 32ft deep the total pressure is about 30 psi and at 64ft deep pressure is about 45psi. This means there’s twice as much nitrogen in her blood and tissues at 32ft and three times as much at 64ft.
If you are on the ground at sea level, the pressure in your lungs is also about 15psi. When you breathe in it is slightly less, and when you breathe out it is slightly more. This small difference in pressure is what makes the air move in and out of your lungs.
Because the human body is flexible, when subject to an external pressure, that pressure is experienced equally throughout the whole body. This comes from pressure on the skin - it doesn't come through the airline (though that does need to be at the same pressure of course). If you want the pressure inside to be lower than the outside pressure then you need a rigid encasement such as a submarine or bathysphere where that exterior can support the pressure difference. You can see how an air-filled balloon expands as it rises in this  video (from about 3:25)
The pressure in our arteries is a little higher than outside pressure; on average that’s about 100 mmHg or about 2 psi, as the heart has to pump blood around the body. It’s also a little higher in our tissues, as the cell walls have to keep their contents inside against the force of gravity etc. Healthy human lungs have a surface area about equal to the size of a tennis court which allows for efficient diffusion of gases across this barrier. However it takes a much longer time for gases to diffuse out of tissues into the blood stream and be conveyed to the lungs. A bubble of air inside water has a higher pressure inside than that in the surrounding water due to surface tension of the surface of the bubble which is trying to contract, the smaller the bubble the higher the pressure. This means that, in general, dissolved gases have any easier time diffusing out of a cell than forming a bubble.
According to Navy diving tables the maximum time at 60ft is about 55min without the need for decompression. But ascent should be slow at about 0.5ft/s. Longer dives at this depth do require decompression protocol. wikipedia as illustrated by Naval sea systems command - US Navy Diving Manual, Revision 6. SS521-AG-PRO-010, Public Domain
As I said, this whole process is slow, so that if there is a sudden change in outside pressure dissolved gases will nucleate and form bubbles. This can happen even when the outside pressure is originally atmospheric. For example passengers flying at great height in a plane with a pressurized cabin can experience DCS if there is a sudden decompression, as when a window blows out. So reducing the external pressure on the lower half of the body will only make the situation worse as dissolved gases will rapidly form bubbles there.
The same thing can happen to fish! recent news
Edit:  According to David Hammen’s answer to this question air on ISS there is no chance of DCS when using pure oxygen at 30kPa. which astronauts do in their EMUs. It’s nitrogen which is the big problem. They do however have to reduce the nitrogen levels in their blood before donning these suits as air in the ISS is at atmospheric pressure with 79% nitrogen.
Also, high pressure oxygen is the best treatment for DCS. Hyperbaric Oxygen Therapy
In case of rapid decompression of the EMU due to accident or failure, getting back inside the ISS would seem to be the priority.
Good luck with your suit design.

A diver who goes to 60 feet can stay underwater for about 45 minutes and ascend at a rate of half a foot per second (not per minute) with a three-minute stop at 15 feet - about 40 minutes down and 5 surfacing. Decompression is only required for deeper or longer dives.

@Eonema You're right. I'll correct that.

Your body isn't rigid. All of your blood vessels are under pressure from the atmosphere, from the pressure of the air pushing on your skin which pushes on the underlying tissue.
When nitrogen or anything else is dissolved in blood, it's dissolved under that atmospheric pressure. If that pressure suddenly drops, it bubbles out, just like the bubbles in a carbonated soda that is under pressure until you open the can. Those bubbles happening in blood vessels is bad because it blocks them. That's the bends.

That makes sense. But skin is gas-tight by itself. From what I've read about research into mechanical counter-pressure suits, it's not like we strictly need to be surrounded by an atmosphere so much as we need pressure (and air to breathe).

@Mia You can squeeze a balloon and increase the pressure inside without any gas moving into the balloon. Your body is a big balloon of biology.

Sure, yes. Swelling and bruising would occur, you'd be generally uncomfortable and in some period of time you'd die. My question is much more specific - would nitrogen come out of solution and form bubbles in your bloodstream? This is the documented mechanism of decompression sickness and it is not clear to me if it would still occur if pressure in the lungs remained unchanged.

@Mia No one would ever be able to do your experiment, it would have disastrous consequences for all of circulation. But yes, if you had just a closed system of blood with dissolved gasses in a tube and reduced the pressure, bubbles will form. That's the mechanism. It has nothing to do with the lungs. No source is talking about bubbles forming because of the lungs. The quote you have is about the other place gas can go to not produce bubbles which is that it is breathed out if the change is slow enough.

Fair enough, thank you for your responses. My mind has been on questions of pressure suit design. Wondering if hybrid designs involving a helmet-volume kept at ~100kPa to avoid the need for pre-breathing and a body-volume kept at ~30kPa for mobility purposes would be possible. It sounds like decompression sickness would still occur. Obviously the body can handle the lower pressures in general since existing designs are ~30kPa throughout the entire suit, but I guess inconsistencies in pressure over the entire body would be too big an issue.

@Mia Diving suits are flexible, they allow pressure in throughout the whole suit just like your skin, just like a balloon. If they didn't and left part pressurized and part non-pressurized, you'd force tissue into the non-pressurized area which would be very traumatic and bad. The alternative is a completely hard body, like a submarine, which can have different pressure outside and in. You absolutely cannot keep the helmet and body at different pressures otherwise you'd have 70kPa of pressure pushing your neck and head into your chest cavity.

The least-bad thing that would happen is no blood flow to the head in that circumstance; hopefully that would kill you before everything else happened.

Ah to be clear I'm talking about suits for surviving low pressure, if that makes a difference for context. The current EVA suits used by astronauts are kept at 30kPA of pure oxygen for flexibility purposes. I've also been looking at the design of mechanical counterpressure suits. https://en.wikipedia.org/wiki/Mechanical_counterpressure_suit

@Mia Exact same problem with low or high pressure; with pressure, it's differences that matter for the physics, mostly (unless you're talking chemical reactions or temperature). Counterpressure suits don't attempt to apply a different amount of pressure in different compartments; even if there's a rigid helmet the pressure is allowed to equalize between compartments (and it will equalize, so you'd rather that equalization happen by air moving rather than body parts).

Thanks again for your answers, Bryan. For what it's worth I'm not the first person to think of looking into this, I just found a study done on this at UC Berkley in 2001. Here's a link to the PDF if you're curious: https://www.lpi.usra.edu/publications/reports/CB-1106/ucb01.pdf


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Can snake deposit venom while drinking?
When a venomous snake drinks, does it deposit even trace amounts of venom into water?
I understand that "drinking" and "biting"(attacking) involve different reflexes and muscle complexes, so it would probably not be "natural" for a snake to deposit venom while drinking, so the question is probably more about the "hermeticity" of the venom sacs/glands - does venom seep out.
Thank you.


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How are plant meristems free from viral infection?
My textbook mentions an application of tissue culture; A meristem extract from an infected plant (both apical and axillary work) can be used to grow a virus-free plant in vitro. But what makes these meristematic cells special so they don't get infected?
Edit:I read an article on a protein called WUSCHEL that inhibits the prodction of viral proteins (by halting protein production altogether). So is this protein the main reason?

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. Please also note the homework requirement - so tell us what you know about this topic - hint: there are lots of answers easily accessible by searching.


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Chromosomes in humans and chimpanzees
I am reading a book titled 'Critical Thinking Skills for Dummies' by Martin Cohen, in which I came across this passage:
'Although humans share 98 per cent of their genes with chimpanzees, they share precisely 0 per cent of their chromosomes -and chromosomes are what actually do things.'
Is this correct?

List item

If he did, that's a really dumb thing to say, and there is an extreme lack of critical thinking present in that statement. Chromosomes are a bit like houses, houses where genes live. Genes are "what do things"; chromosomes themselves are inactive. Here you can see an example of a human and a chimpanzee chromosome, and an brief explanation of chromosomes and genes.

@anongoodnurse that (that chrs are inactive) is an odd statement. Chromosomes and genes are not distinct things, genes are DNA sequences, and chromosomes are large stretches of DNA sequence. Genes are chromosomes in the sense that my arms are me. So no, chromosomes are not inactive. Perhaps a closer analogy would be that chromosomes are books that contain many sentences. Some of the sentences are nonsense, and some carry meaning (genes). Yes, it is the ones that carry meaning that "do things" but the book isn't inactive as it is made up of the bits that carry meaning and those that don't.

Minor nitpicking aside, I have to agree with anongoodnurse's sentiment: that sentence is nonsensical. I don't understand how the author decides to quantify whether or not chromosomes are "shared". Is that in terms of sequence? Gene complement per chromosome? Order of the genes? Can you clarify what the specific claim you are asking about it? The statement as a whole is neither true nor false because it is nonsensical. Is there some context to clarify?

@terdon - Your analogy is better, true. Chromosomes are "inactive" in so far as switching to your analogy) the book is closed. You can't read a closed book; it must be opened in order to have phrases read and meanings understood. So, too, must the chromosome be "opened" to let the genes out. The book houses (and contains) the words. Chromosomes house (and contain) the genes. But yours is the better analogy. Regardless, we are both aware of the stupidity of that statement alone. It may be explained further, but I couldn't locate it with searxching.

Perhaps the author is suggesting you should critically think to ignore his book.

This might be an exercise in logical fallacies and arguments. I wish we had the exact wording so that the context could be read. All we have is a paraphrase. The author doesn't seem to be an idiot, although he appears to deny climate change as an argument from authority...

@anongoodnurse or terdon (sorry only 1 tag allowed), I do think it would be helpful if one of you could write an answer, since this is a good faith question and there is a clear answer. Then that could settle it. No one seems to be of the opinion that this is a homework-style question, if only due to the incredulity that we collectively feel towards what this Cohen character is saying.

@terdon see above

@MaximilianPress I can't answer since I don't understand the question. If the question is "is it actually chromosomes that 'do things'?" then it isn't even answerable since that is a nonsensical question. If it is "do humans and chimps share their chromosomes", then we would need an explanation of what is meant by "shared" in this context. In its current state, the question is too unclear to be answerable.


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Why does these confocal images show concentric circles?
I recently got this confocal microscopic image from my microscopy facility. I am unable to understand why these concentric circles are there. They look like out of focal fringes in conventional microscopy, but this is from a confocal as I mentioned. (It is only appearing in red channel, if that provides a hint.)
They are present in several images toa varying extent.

Welcome user 80133. Could you provide a few more details such as the subject, medium and the approximate magnification or some other idea of scale. It seems like some artifact of refraction due to droplet surrounding the subject, but we'd nee more details.

“Does this” or “Do these”. A basic feature of English grammar is number agreement between subject and verb.


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Relation of pH and amino acids in microtitr assay
I am testing a Biolog plate (https://www.biolog.com/products/metabolic-characterization-microplates/) in which the wells test for the optimum pH at which my bacterium grows. Aside from having a range of pHs (3.5 - 10), two pHs (4.5 and 9.5) are tested with a range of amino acids (and some other compounds such as urea).
My question is why would there be any interest of testing these amino acids at two different pHs. My guess is just to test for any oligotrophys but on the other hand they could have then prepared these assays with any other set of random compounds. Is there any specific to amino acids and pH that I am missing.
Here is the picture of the different compounds tested in the micro-titter plates.


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Converting m/s to body lengths / s
I am trying to calculate speed of fish in body lengths / s. As of now, I have speeds for each of my individuals in m/s. To convert each individual fish's speed in body lengths / s (bl/s; using each fish's body length), from m/s, I assume I can simply divide each m/s value by the body length of the fish.
For example:
I have a speed of 0.35 m/s, Fish A's length is 0.66 m. To convert into bl/s I should divide 0.35 / 0.66 to get 0.53 bl/s.
Is this correct or is there some kind of unit conversions that come into this? Since it's relative to the fish's length, I assume this is ok? If this isn't correct, would you please show me the correct way to calculate this?

For all unit conversions, you want to learn to multiply by ratios that are equal to 1 and make things cancel. So if you have units of "x/s" and you want to express in "y/s", you need to multiply by "y/x" so that the xs cancel. To make it work, you need y/x to be equal to 1. For example, if x = 1 meter then you could use y = 100 centimeters. If you want y = 1 body length then you need x = ____ meters, whatever makes it equal to y. Whatever units you choose, when you do this you're always multiplying by 1 overall which we know doesn't change the actual number.

Thank you for the response.... so if I have 0.35 m/s and want body length (which is expressed in m) / s, I need to multiply by y/x which would be 1 body length/0.66 m... when you cross multiply this gives you 0.231 bl/s? Is this correct? What did I do wrong initially? I thought that since body length is just a ratio of 1 m, I would just need to divide to see that ratio through.

No no, no "cross multiplying". You did it correctly the first time:$$\pu{0.35 \frac{m}{s}}=\pu{0.35 \frac{m}{s}}\times \underbrace{ \frac{\pu{1 bl}}{\pu{0.66 m}}}_1=\pu{0.53 \frac{m}{s}}$$

@Domen did you mean 0.53 bl/s? (even though in this case bl is measured in m)

Arghh, yes, of course, my mistake :)

Thank you so much!


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How can I introduce Na+ in cells?
If in a solution with living cells Na+ ions are included do the cells intake it only because of the concentration?

May I suggest you look up ion transporters and ion regulation and how they work.

Also maybe explain what you're trying to accomplish.

@BryanKrause I want to feed the cells with Na+ so they get a charge. So I think to pour more Na+ in the solution. Will they eat it?

@bob1 I don't want to get into some difficult stuff. Just want to know the result and practical ways to put charge in a cell.

@Mercury In that case you need to include that information in the question - because we don't know what you want to do and why. I read it as a question on physiology of ion uptake, not a practical question.

Neurophysiologists do this with patch clamp, placing a glass pipette against the membrane and using suction to pierce it; you need to gain access to the cell physically.
Doing this will fill the cell with whatever solution you have in your pipette; you'll need to use something similar to what the cell has inside, but you can tweak it a bit, like adding more sodium. If you just want to change the charge of the cell, you can do that with your patch clamp amplifier directly.
There is no other way to do this. Ions move by diffusion through membrane pores called ion channels; any positive charges moving across a membrane carry with them a positive charge that will repel further positive charges from moving across that membrane. If you use the patch clamp technique to tweak things, ions will keep moving according to their charge and permeability; any space that you make more positive will result in positive ions leaving that space and negative ions coming in.
You will kill cells if you disrupt things too much. Most of the energy that biological systems use goes, in one way or another, towards maintaining the specific environment that a given biological cell or organism is adapted to.


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How do you re-adjust gaze coordinates after bad eye tracking calibration using Matlab?
As a beginner with oculometric data pre-processing (in children from 2 to 12 years old), I would want some advice from the community! :)
Using a Tobii Pro Fusion Eye tracker (250Hz), children are asked to watch stimuli like objects, avatars, and faces (4s per stimulus). My goal is to calculate, in a series of areas of interest which correspond to an x-y coordinate range for each trial, when and where the first fixation occurred, the duration of the first fixation, and the total visit duration/the total time spent of each corresponding AOI, for example. AOIs are, for example, the nose, the mouth, and the eyes of faces.
As I work with young children, I sometimes have lousy calibration (even with our best effort with the child!), and the recording takes place without calibration or with "bad calibration".
With Matlab, I am trying to re-adjust the gaze position to be the most loyal to where the child looks during the apparition of the stimuli because "bad calibration" affects where the children look.
I was wondering if the best way was to either re-adjust the gaze position as a function of the precision and validation (in degree) of the calibration or as a function of the interstim, considering that children look at it correctly (the interstim is a black cross appearing 2 to 3s before the stimuli).
As I am new to this, I am all ears for some tips :)
Thanks to all the community for future advice!
Best, Camille

Unfortunately I worry that not many people in this community will have expertise here! Which is too bad as it's a good question. However, there is a Neuroscience Stack Exchange that seems to have a variety of questions/answers on this topic. I'm going to flag your question for migration there.


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Action Potential
I was wondering what exactly initiates an action potential? I understand that for depolarisation to occur, the membrane potential must first pass through the threshold potential, but what process leads to the membrane potential being raised to the threshold potential in the first place? I suppose this question would pertain more so to nerve cells since in muscle cells the membrane potential is raised due to the opening of nicotinic receptors and the influx of cations.

In addition to the duplicate which answers your question, I would note that a typical textbook progression introducing neuroscience is to go from resting membrane potential to excitable membranes (= action potentials) to synaptic transmission, so if you're learning from a textbook you may just need to keep going to the next chapter.


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Receptor tyrosine kinases: Clarification about what is meant by stabilization of the receptor
I am reading a journal paper. This paper focuses on how neural cell adhesion molecule (NCAM) interacts with fibroblast growth factor receptor 1 (FGFR1) and promotes its stabilization.
When FGF binds to FGFR1, the receptor gets internalized and degraded by lysosomes.
In contrast, when the soluble ectodomain of NCAM binds to FGFR1 the receptor gets internalized and recycled back to the cell surface, resulting in sustained signaling.
I asked in another question, what is meant by the stabilization of a receptor, and the response stated that it means the receptor stays in the plasma membrane and doesn't get re-internalized.
However, in the case of this paper, it seems that stabilization means that the receptor doesn't get degraded after it is endocytosed.
What exactly does 'stabilization' mean in the context of a cell-surface receptor? Any advice is appreciated.

I would look at their methods: what are they measuring? That's what they mean by stabilization.


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How to identify unknown RNA species that copurified with protein
So I have been studying an E. coli protein. As the first step I purified it in a pretty standard way - overexpressed it in BL21 DE3 cells and placed it in an ion exchange column, followed by size exclusion chromatography. Interestingly on the size exclusion column the protein fraction from IEX seperated into my protein of interest plus a very defined RNA species (which on a gel ran at ~500kDa). our university has a sequencing service that can accept DNA. Would anyone have suggestions as to how I can identify this  I tried RTPCR for this protein using random hexamer primers but to no success.

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on how this site works and what we do here.  We probably need a few more details on your experiment - How did you identify it as RNA? How do you know the RT-PCR failed? Do you have access to a MinION device?


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Why do monoclonal and polyclonal antibodies behave differently as labeled secondary antibodies?
According to the MBL guide to generating antibodies, the differences between monoclonal and polyclonal antibody extend beyond the fact that the latter is heterogeneous, binding to various epitopes for the same antigen. According to the source, monoclonal and polyclonal antibodies behave differently with respect to labeling:

Labeled (secondary) antibodies:
Similarly, only one antibody molecule can bind to a primary antibody molecule if the secondary antibody is a labeled monoclonal antibody. Whereas multiple antibodies can bind to a primary antibody molecule if the secondary antibody is a polyclonal antibody.
Consequently, polyclonal antibodies provide a higher sensitivity of detection (amplification of the signal) and, therefore, are commonly used as a secondary antibody.

What is the mechanism for this difference?

The mechanism for this is (as stated in the first sentence of the quote) that in a monoclonal antibody all antibodies bind the same site (epitope), whereas in a polyclonal antibody you have a mix of antibodies that all recognize different parts of the antigen. Therefore, multiple polyclonal secondary antibodies will bind the primary at different sites, while in a monoclonal secondary there is only one site in the primary antibody that is bound.


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Looking for research related to burising sensitivity and rate of heeling
Are there studies/data on the potential correlation between how quickly a body heals itself and how prone to bruising the body is?
I've been reading that oxygen is needed in the healing:

Wounds need oxygen to heal properly. Exposing a wound to 100% oxygen may speed healing. Hyperbaric oxygen therapy can be done in a number of ways. It can be given in a special type of room called a hyperbaric oxygen chamber. -Hyperbaric Oxygen Therapy for Wound Healing

And that bruising essentially is the pooling of blood from damaged blood vessels.

Bruises occur when blood vessels break, due to some kind of force, and leak blood into areas under the skin. -Mount Sinai: Bruise Information

This has led me to hypothesize "On average a person with a higher sensitivity to bruising will heal faster than a person with low sensitivity.". This hypothesis was created out of the idea that due to the increased concentration of oxygen found at the wound location (caused by the trapped/pooling of red blood cells), the damaged cells will be able to utilize this increase to heal quicker.
I'd like to do some research to determine if this hypothesis is true, plausible, unlikely, false or unknown.
If the hypothesis is true then some blood vessels might be more prone to leak blood when damaged. This trait would have been selected for, because it would help the initial healing process by increasing the oxygen concentration at the wound location.
This is just my hypothesis and I'm looking for information to guide my research.

Why do you think that the blood at a bruise site has more O2 than elsewhere in the tissue? Read up on responses to bruising by the body...

I do not believe that the blood at the site has more O2 than blood anywhere else in the body. I believe that a higher concentration of blood forming in a location normally without blood will increase the density of O2 in the area.

If you think about the biological processes that go on - why does a bruise appear? Why does it not disappear in a short time-frame (as it should if blood flow happens...) What happens to the O2 in the blood cells? What happens if the blood flow is stopped (tied in to q 1 and 2 above) - where does the O2 go and is it replenished? BTW use the format @ followed by username to notify someone you've made a response to a comment e.g. @Tolure will notify you of a comment.

@bob1 the red blood cells get trapped after the body heals the damaged blood vessel. The red bloods cells give the bruise its redish colour. After the red blood cells break down the oxygen is released to the area and the bruise changes colour. Now I will accept that there might not be a mechanism to allow for a damaged cell to take advantage of this. If so please draft an answer stating as such.

No this is homework for you - I think your understanding of the timing of events is off. Blood gets trapped almost immediately. The body uses up the O2 (normal cellular respiration) and changes colour (that's not due to respiration, rather degradation of the RBCs) - so why would there be more O2 at the bruise than elsewhere?

@bob1 would you agree that a volume of oxygen-rich hemoglobin has a higher concentration of O2 than the same volume of tissue? If so why would the concentration of O2 in an area not change when the ratio of tissue to hemoglobin changes due to the pooling of blood caused by bruising?

@Tolure You need constant circulation of blood for it to stay oxygenated. Blood just sitting there isn't resupplied with new oxygen.

Agreed but I'm only looking at the initial state. Where the hemoglobin still had oxygen. Once the hemoglobin have released their oxygen then yes I agree the hemoglobin wouldn't help in the healing. Now when the trapped hemoglobin release their oxygen that they already had prior to being trapped could it help the healing?

@Tolure How fast do you think the O2 from the pooled blood will be gone? How fast do you think healing processes are?

@bob1 O2 Used up: Very quick and Healing: very slow.
I also know that sometimes just a little benefit now can have compounded benefits later on.


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Radiocarbon dating tooth from living person
Would it be possible to use radiocarbon dating on a tooth, lost by a person while they were still alive, to determine that person's birth year?
Imagine an adult who loses a tooth for whatever reason at age 40, but lives to age 100.  Would that tooth suffice to approximate their birth year?
Edit to include:
In an effort to not waste people's time reading a long question, I erred on the side of too little information.

Yes, I'm very familiar with the Wikipedia article on radiocarbon dating.
I have read the linked similar question and all of its responses.

Which leads to these specifics:

Is one adult human tooth adequate for radiocarbon dating purposes?
Could such a tooth from a period of 200 to 700 years ago be dated to within a small enough window to make a difference, i.e. the window would be smaller than 500 years.

Delving into that, I found a number of articles.  This one on radiocarbon dating on recent human remains was partially helpful:  https://nij.ojp.gov/topics/articles/applying-carbon-14-dating-recent-human-remains
TL;DR:  For people who acquired adult teeth between roughly 1965 and 2030, the technique will work, thanks to unusual amounts of C14 in the environment as a result of nuclear weapon testing.
This article suggests the ability to date samples of a similar recent vintage, though I did not purchase the article and read the whole thing:  https://www.cambridge.org/core/journals/radiocarbon/article/abs/application-of-radiocarbon-dating-to-forensic-investigation-and-evaluation-of-formaldehyde-influence-on-radiocarbon-age/1B02FEF83B5D1F5E11F8E02D9550A57D
This is sadly not useful for me, with my teeth samples carefully preserved from someone who was born in 1552.
It looks like the answer to my question is "no" -- C14 dating is too imprecise to be useful for such a recent and short time span.  But this is my non-expert reading of the various articles mentioned and linked.

Possible duplicate: https://biology.stackexchange.com/q/24084/5198

@John Make your comment an answer and I'll mark it as the answer I was looking for.


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KEGG map01100: Is this ectomycorrhizae or arbuscular mycorrhizae
Just as background mycorrhizae are fungi and split into two groups ectomycorrhizae and arbuscular mycorrhizae (AM). Taxonomically these fungi groups are very distinct. Ectomycorrhizae belong to the phyla Basidiomycota and Ascomycota, whilst AM are Glomeromycota.
I am really interested in the KEGG map01100 (metabolome map) called "mycorrhizae". The question is

What phyla is the map taken from?
Where do I find out the information/reference about how (and where) this map was constructed from?

I don't know the exact answer, and a quick click around didn't yield an obvious result for the overall pathway. The KEGG annotation process is manual and may not be easy to reconstruct overall (though is generally quite high quality).
However, if you click the "Help" it tells you that there is a reference for the ko pathway view. I wasn't able to actually locate this, but I was able to follow the ko pathway view to the gene orthology view for specific enzymes, which in turn tells you which organisms it's represented in, which you can click through on to find, in this case, an Ascomycota.
I'm sure that there is a way under the hood of the KEGG API or the KEGG database view to pull this information for everything. I imagine that you will likely find a mixture of phyla because they try very hard to generalize the broad biological categories. But that's a guess!
At worst, you might be able to scrape the website to get a reasonable guess for the various enzymes of which phylum they mostly come from.
I would guess that you could ask someone at KEGG and get a more satisfying answer! I'd be interested to see how their sausage gets made as well.

Thanks @MaximilianPress the link you highlighted is cool https://www.genome.jp/entry/K19634


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How do animals that live in dens keep the dens from flooding?
When it rains heavily or flooding starts what do animals like foxes,wolves, and any other animal that makes a den or lives underground do.? Do their den's/home's flood?

this depends a lot on the animal but generally the shape or location of the den. Simply don't build dens in places prone to flooding, otherwise the shape of the den works.
Foxes for instance which do build dens is places were flooding can occur build V shaped tunnels to their natal dens, so water would have to run uphill to reach the places they actually use. Beavers likewise dig there dens upwards.
here is picture from something completely unrelated that can help.

https://www.jstor.org/stable/41713116


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Mitochondrial shape and function
I was wondering how can mitochondria come in different shapes and sizes? And why are they always shown as ovals on textbooks?
p.s. I would appreciate any suggestions for wider reading on mitochondria and cellular biology as well.

Welcome laerningsheep. Please take our [tour] and read-up in the [help], especially the [ask] section, taking particular note of the requirement that questions should show their prior research. You can then [edit] to show us what you searched, found and where you got stuck. Perhaps start with Mitochondrial evolution to get an idea about where we think they come from at present.


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How is the zone of inhibition formed in disk diffusion?
Question
How is the zone of inhibition formed in disk diffusion?
What I mean by the formation of the zone of inhibition is not the ultimate visibility of such zone but the circumstances that result in the matter becoming settled and further incubation being merely done to reveal the endpoint of the experiment:

In general, the entire process is completed and the position of the
zone of inhibition determined within the first few hours of
incubation.
Barry AL. Procedure for testing antibiotics in agar
media: theoretical considerations. In: Lorian V, ed.
Antibiotics in laboratory medicine. Baltimore: Williams &
Wilkins, 1980:1–23.

Prior research

The zone of inhibition is formed when a critical concentration of drug
(that amount that is just capable of inhibiting microbial growth under
the test conditions) reaches, for the first time, a density of cells
too large for it to inhibit. The size of the zone of inhibited growth
is determined by the distance that the critical inhibitory
concentration can diffuse into the agar medium before a particular
density of cells is reached. Thus, the diffusion test is actually a
race between the drug diffusing from the reservoir and the
microorganisms initiating growth.
Barry AL. Procedure for testing antibiotics in agar
media: theoretical considerations. In: Lorian V, ed.
Antibiotics in laboratory medicine. Baltimore: Williams &
Wilkins, 1980:1–23.

I can't get to understand what's a/the critical concentration.
How I understand the matter:

The zone of inhibition is formed when a concentration of drug reaches,
for the first time, a density of cells too large for it to inhibit,
and any additional drug concentration reinforcement arriving from the
reservoir won't make a difference.

if my understanding is right, how does it go with the prior explanation?

Something important that I don't see mentioned in the answer below is that you generally cannot determine the minimum inhibitory concentration of a drug by measuring the inhibition zone of a disk diffusion assay.

Read the last part of my answer (at-least).

I have improved this part, could you please check it?

Despite its simplicity, the disk diffusion test is based on
sophisticated physicochemical principles governing the dynamics of
diffusion of antibiotics simultaneous to bacterial growth in an agar
system.

Wanger, A., Disk diffusion test and gradient methodologies. Antimicrobial Susceptibility Testing Protocols, 2007
Inhibition
The process of keeping the cell mass in a given area constant.
Critical concentration
A critical concentration is the antimicrobial concentration required to inhibit a certain cell mass in a given area decisively so that it's irrespective of any future decrease in this concentration due to diffusion of the drug further from this area.
It seems to me that's why rapid AST (results being read immediately after the appearance of visible growth) can't be performed in some cases: the inhibition zone becomes smaller with further incubation as the drug concentration becomes less than the critical concentration for the current cell mass at the edge of the inhibition zone:

Occasionally there is another faint inner ring of delayed growth that
represents viable cells initially inhibited by the concentration of
drug at that point. As incubation continues, inhibited cells will
eventually grow when the concentration of drug is reduced either by
continued diffusion outward or by deterioration of the drug at
incubator temperatures. An inner ring of delayed growth is most
commonly seen with drugs which are primarily bacteriostatic. As
incubation continues the inner ring of delayed or partial growth
becomes increasingly visible and thus it would appear that the zone of
inhibition becomes smaller as the incubation time continues. It is for
this reason that the period of incubation must be standardized and
held constant.
Barry AL. Procedure for testing antibiotics in agar media: theoretical considerations. In: Lorian V, ed. Antibiotics in laboratory medicine. Baltimore: Williams & Wilkins, 1980:1–23.

Critical mass
A critical mass is the cell mass required to counter a certain antimicrobial concentration in a given area decisively so that it's irrespective of any future increase in this concentration due to the diffusion of more drug concentration to this area.
The Critical concentration
It's a critical concentration for the cell mass found at the outermost point inside of what's going to be the zone of inhibition at a certain time called the critical time.
The Critical mass
It's a critical mass for the antibiotic concentration in the point just outside what's going to be the zone of inhibition at a certain time called the critical time.
Formation of the zone of inhibition at the critical time

A zone of inhibition is formed when a critical concentration of drug [the critical concentration]
(that amount that is just capable of inhibiting microbial growth under
the test conditions) reaches, for the first time, a density of cells
[the critical mass] too large for it to inhibit.
Barry AL. Procedure for testing antibiotics in agar media: theoretical considerations. In: Lorian V, ed. Antibiotics in laboratory medicine. Baltimore: Williams & Wilkins, 1980:1–23.
The position of the zone of inhibition is determined at a point of
time [the critical time] when the critical concentration of drug reaches, for the first
time, a density of growing cells too large for it to inhibit. When the
antimicrobic is added at the time incubation is started, the position
of the zone of inhibition is determined after a critical time.
Barry AL. Procedure for testing antibiotics in agar media: theoretical considerations. In: Lorian V, ed. Antibiotics in laboratory medicine. Baltimore: Williams & Wilkins, 1980:1–23.

MIC vs Critical concentration
In broth microdilution, the MIC has access to all the cell mass equally and immediately, unlike in disk diffusion, where critical concentration reaches its coressponding mass gradually as time passes. This causes the fact that any cell mass will be subject to a subinhibitory concentration of the antibiotic before the inhibitory critical concentration. I think this needs to be considered when trying to relate the two factors.
To add, critical concentration is a concentration gradient not a concentration per se like MIC: as for the aforementioned reinforcements and outward diffusion.

I removed the part that included naive conclusion about MIC being equal to the critical theoretical being the most adjacent to the disk.

Generally antibiotics don't actually kill the bacteria, all they do is inhibit growth so that you don't get any new cells formed.
Thus, if you have a drug diffusing away from the disk, at some point the drug will reach a concentration that allows growth of standard concentration (often 0.5 McFarland) of the bacteria applied to the plate. Even if the zone of high concentration extends out further from the disk due to diffusion, these bacteria will still be there (remember inhibited, not killed), so you will see these bacteria and have determined the zone of inhibition.
Now, you might be thinking this should result in a halo where you don't get much growth but still get some before the drug reaches inhibitory concentration. In practice, you do see this, but it tends to be minimal for the reasons below:
The concentration at any given point is dependent on the square of the radius of the zone (area = pi*r2. To reach a higher concentration you need a lot more drug to shift the point. For a made up example - if you have a zone of inhibition with a diameter of 2 cm (i.e radius of 1 cm). To get this same point out a further centimetre, you would have a radius of 2 = 22 = 4x as much drug at each point around the circle. (I'm aware there's some problem with this math, it's just an illustration of the problem).
Diffusion rates in agar are also slow; in the order of 1-10 micrometres per second IIRC. This works out to be somewhere in the range of 100-1000 seconds (1.67 min to 16.67 min) per millimetre, which, in combination with the need for much more drug per increase in radius, results in the sharp zone of inhibition seen.

There are bactericidal antibiotics, like the beta-lactam antibiotics (and several other). They affect the formation of the cell wall leading the bursting of the cells.

@Chris For sure, though I didn't have the B-lactams in that group in my head; I knew they inhibited cell wall synthesis, just thought that inhibited division; time to go back and review my textbooks methinks.

Why would you think it would matter for this experiment that the antibiotic kills or inhibit the bacteria? Maybe it's not that the antimicrobial inhibits bacteria instead of killing them that results in lawn growth in areas outside the inhibition zone even if post inhibitory conc reaches these areas. If my reading is right، there is a critical cell mass for every dynamic antimicrobial conc that if reached, this conc and the highest it could reach as a result of reinforcements arriving from the disc, won't be able to counter the growth rate in this area.

I think it goes like this: For every cell mass of a certain organism, there is a critical conc of antibiotic, if this conc reaches this mass, it would result in inhibition of growth. Then each spot in the plate could be thought of a gradient itself for different antibiotic concentrations, not just the disc. Then and in the same way, for each conc gradient, there is a critical cell mass, that if the mass in the vicinity of this gradient reaches, growth won't be inhibited.

These multiple gradients are themselves being changed by the fact of reinforcements arriving. I think that what a dynamic gradient means.

@FreezingSoul Then each spot in the plate could be thought of a gradient itself for different antibiotic concentrations, not just the disc. No, the gradient is dependent on the disk. The antibiotic kills/inhibits growth so you don't get growth in those areas. The cell mass at each area is defined by your McFarland standard spread on the plate, so it should be consistent across the plate.

Read my answer, please. I will try to refine it over the time.


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How do Action Potentials travel in Cardiac Muscle Cells?
From my reading, the action potential is generated by pacemaker cells within the SA node and the conduction system of the heart carries the action potential to the cardiac muscle cells. I was just wondering whether the action potential travels through gap junctions or along the sarcolemma? It would need to travel along the sarcolemma to activate L-type calcium channels during muscle contraction, but how does the action potential actually travel from the SA node to the membrane of the cell? How does it just 'jump' to the surface of the muscle cell?
In addition to that inquiry, when do action potentials travel through the gap junction then? Does the action potential travel through both the sarcolemma and the gap junctions?


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If I increase the permease enzyme in the Ecoli, will that make it take up lactose even though glucose and galactose are present in more amount?
E coli takes up glucose and galactose on preference because those are easy for it to metabolise.
When there's no glucose and galactose available, it takes up lactose and the lac operon genes produce their products ( gene z codes for enzyme beta galactosidase, gene y codes for permease which helps the bacteria take lactose inside, and gene a codes for transacetylase)
So if I increase the permease enzyme, would it be able to take up lactose even though glucose and galactose is present in more amount?

Why would you think it would? How much more do you need it to take up? by how much are you overexpressing permease? what are the enzymatic preferences for these various sugars? Write it all out, and I suspect you'll have answered your own question.


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If you want to understand evolution from a genetics standpoint what are some must reads be it books or textbooks?
The question basically sums it up. I'm looking for books/textbooks that explain evolution from a genetic perspective.

So your question is about your problem, not a problem in biology. I suggest re-reading the [Tour] for examples of the types of biological questions that are on-topic here.

https://en.wikipedia.org/wiki/Modern_synthesis_(20th_century)

For a historical perspective and summary, see here.
For a textbook that works through the math from a very simple foundation, see here. (Felsenstein, J. Theoretical Evolutionary Genetics, 2019).


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Why are sunflower seeds so much smaller than their shells?
I was snacking on some sunflower seeds recently when I noticed the large disparity between the size of the seed itself and the woody shell surrounding it. Why is this gap present? Is there some evolutionary advantage to making a seed pod larger? Or did the seed shrink over time?

I’m assuming the seeds you were eating were roasted and therefore dehydrated. Crack open a fresh seed and see if you observe the same thing.

Ahhhhhhhhhh that would explain it. Thanks!


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Why do different people perceive the colors of the Northern Lights (Aurora Borealis) differently?
A few days ago, I was in Norway with a group of about 20 people. We were fortunate enough to witness an impressive display of the Northern Lights that lasted several hours. The next day, we discovered that while some of us saw the Aurora as clearly green, others perceived it as white or grayish (the split was about 50/50).
Our cell phone photos showed bright greens and reds. I understand that the cameras used long exposure times (about 4 seconds), allowing their sensors to capture much more light than our eyes. However, I’m puzzled as to why different people saw different colors.
Here are a few things to note:

There was no obvious correlation between the colors seen and factors such as age or gender. For instance, I am 53 years old and saw distinct colors that others, both younger and older, could not see.
We were all in the same location, far from city lights or car headlights. We watched the sky for over an hour, so our eyes were likely as dark-adapted as possible.
None of us are color blind.
No one saw the red color that appeared as bright as the green in the pictures we took.

The only somewhat reasonable explanation for the different experiences was the difference in pupil diameter between individuals (a smaller diameter means that less light enters the eye, so scotopic vision may be prevalent). However, it seems that the pupillary light reflex is only a minor part of adaptation to ambient light.
So, what could be the main factor influencing the varied color perception of the Northern Lights?

Remember your cell phone has its own colour balancing too.


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What "most closely related to" means in phylogenetic trees?
Here is a sample phylogenetic tree from a textbook publisher:

We often ask questions like "Which organism is most closely related to the pig, the hedgehog or the cow?" I don't like these particular questions, and maybe that's because I misunderstand what "most closely related" means in phylogeny.
I have been told and have read that the most closest relatives share the most recent common ancestor.  For my question, we would have to say the cow is the closest relative of the pig.  My gut feeling says we cannot say that is truly the case unless we have sufficient DNA evidence.  For example, what if we compare the pig and hedgehog genomes and find, say, 80% match.  We might then compare the pig and cow genomes and find, say, a 78% match.  Would this not mean that the hedgehog is more closely related to the pig than the cow is to the pig, despite the heuristics we have been handing students about reading phylogenetic trees?
Here is an extreme example to make my case:  Is the oldest species of archaea more closely related to humans or to the species of bacteria which most recently preceded the archaea?  If we use the "most recent common ancestor" answer, we must say the archaea is more closely related to the human, but I would find its temporal proximity (and thus likely % of shared DNA) to the bacterium to be a much more convincing argument for relatedness.
Question:  How should we interpret and approach these sorts of questions, or are they bad questions due to their lack of context?

Can you draw out a simplified example where the pattern you propose would occur? Perhaps using just one gene with a short sequence as an example, or imagining genes as something that are collected over time in a lineage the way someone collects rocks. That is, start with a common ancestor of hedgehogs, pigs, and cows, which then goes through changes to result in the hedgehog lineage on one side and the pig and cow on the other, which then branch again to separate pig and cow lineages.

The phylogenetic trees are constructed based on a model that links observations with an ancestral relationship. So I think you need to specify which evolutionary sequence you're considering (as Bryan Krause says above), and which types of observations you're interested in correlating to it. Your question focuses on genetic sequences as the main observations. The whole "Woesean revolution" that established the three domains was based on overturning an older phyologeny based on sequence data. That our lineage includes endosymbiosed bacteria is a different fact of evolution.

@BryanKrause I do not entirely understand your request.  Are you and Ryan saying that a phylogenetic tree is based on only one observation at a time, like only one gene?   Regardless, I'm not exactly sure what it practically means to say "the cow is the closest relative of the pig" in any phylogenetic tree.  What traits, observations, or characteristics are we referring to when we make such a statement?

I'm saying that this is how things actually diverge, one step at a time. So, if you know what the "family tree" looks like (from your picture), I'm challenging you to produce something that looks like your hypothetical numerical relationship. Of course not exactly "78%" or "80%", but I'm suggesting that you run through a hypothetical stepwise process, starting from the common ancestor, and see what you need to do to get that result where you would "calculate" a closer relationship between species not shown as closer according to the tree.

You can do this with a totally made up and hypothetical case; you could start with a gene like AAABBBCCCDDD if you wanted and then change, add, or remove letters one step at a time, or you could use traits/attributes as long as you modify them stepwise. Re-create something like the process that would create these relatives as long as you follow that branching pattern.

Of course it's totally up to you if you actually want to do this exercise or not, but if you do and spend some time on it I think it'll help you understand the answers and better yet understand the whole process a lot better.

@Bryan Krause:  I tried your exercise, and I run into the same problem.  Let's say, for the sake of argument, that the hedgehog has gene AAABBBCCCDDD, but the branch leading to pig, whale, and cow has gene AAABBBCCDDDD, then the pig has AAABBBCDDDDD while the other branch toward cow and whale gets AAABBBCBDDDD.  The cow then gets AAABBBDBDDDD and the whale gets AAABBBBBDDDD.  The pig and hedgehog have 2 letter differences, and the pig and cow also have 2 letter differences.

@Bryan Krause: 2nd scenario: Let's say that the hedgehog has gene AAABBBCCCDDD, but the branch leading to pig, whale, and cow has gene AAABBDCCDDDD, then the pig has AAABBDCDDDDD while the other branch toward cow and whale gets AAABBDCBDDDD.  The cow then gets AAABBDDBDDDD and the whale gets AAABBDBBDDDD.  The pig and hedgehog have 3 letter differences, and the pig and cow have 2 letter differences.  This implies the pig is closer related to the cow.

@Bryan Krause:  Final scenario:  Let's say that the hedgehog has gene AAABBBCCCDDD, but the branch leading to pig, whale, and cow has gene AAABBBCCDDDD, then the pig has AAABBBCDDDDD while the other branch toward cow and whale gets AADBBBCBDDDD.  The cow then gets AADBBBDBDDDD and the whale gets AADBBBBBDDDD.  The pig and hedgehog have 2 letter differences, and the pig and cow have 3 letter differences.  This implies that the pig is closer related to the hedgehog.
Summary:  I'm not sure how this exercise helped, as I can generate any possibility.

Let us continue this discussion in chat.

Phylogenies are an attempt to answer precisely the question of what things are most similar, where "similar" can mean one of a number of things. In statistical terms, a phylogeny is a hierarchical clustering of available organisms based on some similarity criterion. This attempts to make use of second-order information to make guesses about closest relatives based on more than just pairwise similarity; pairwise similarity can give you incorrect answers due to convergent evolution / homoplasy.
A phylogeny based on mitochondrial DNA only will differ from a phylogeny based on full proteome sequences, will differ from a phylogeny based on morphological characters, and so on and so forth. These are all different measures of similarity with advantages and disadvantages. We can further pass these data through one or more models of how the data in question might evolve through the tree. These might include the maximum parsimony model based on Jukes-Cantor distance, maximum likelihood based on the F84 model, or something else.
I believe that the specific measurement that you would be most interested in is the branch length. Branches in phylogenetic cladograms are calibrated to show evolutionary distances according to the evolutionary model fit to the available data.
If you are interested in the nearest relative, you may therefore simply measure the length of the branches differentiating any two tips of the tree. Whatever path is shortest from a tip (organism) $A$ to any other tip will be the nearest relative of tip $A$.
This provides an unambiguous method of identifying a closest relative in a tree. Of course, it does not account for organisms that may be missing from the tree that you consider!
For a clearer guide on reading phylogenetic cladograms, I would suggest this resource.

The common scientific figure of speech is "The closest living relative", because the species are like a puzzling family tree, a phylogenetic tree. We can also theorize about a well documented fossil as "the closest known relative".
We can also use close relatives in a plural and general sense:
The closest living relatives of hyenas are mongooses and civets.
The red panda is most closely related to skunks and raccoons.
Armadillos are most closely related to sloths and anteaters.
It's an interesting and practical way to reason about the tree of life. It is best measured with genetic similarity.
Some species have mysterious ancestry, sea cows, red pandas, hyenas, and so it's useful and interesting to know what family of species they belong to.
The notion of relatedness can be referred to as genetic distance. To research biology trees on the web it's usually best to search images i.e. "amphibian phylogeny"
This notion indicates the evolutionary relationship and genetic similarity between organisms, highlighting their proximity on the evolutionary tree.


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Are there animals which produce sound through direct muscular oscillation?
Obviously, muscles are involved in producing sound, but usually not directly. I.e., the muscles that control human vocal cords do not actually vibrate the vocal cords--a different set of muscles forces air past them, and the moving air makes them vibrate. Rattlesnakes use muscles to oscillate their tails, but the sound comes from rattle sections hitting each other, with frequency components much higher than the tail oscillation. Some insects have muscles directly attached to a tympal, but the sound comes from individual ribs deformity, again unrelated to the frequency of muscle contraction.
So, are there any animals that produce sound like a speaker, by directly causing something to oscillate at the intended frequency by contracting and relaxing muscles to move it with no intermediate steps?

Would hares stamping on the ground count, or must the sound be directly coupled with the air and continuous?

As I understand it, crocodilians may be a candidate, but from what I can find, there's little known directly about how their vocalizations are produced; particularly the low growl (circa 8-10 Hz) might fit.

@JiminyCricket. Stomping on the ground feels like same category as snake rattles. The sound comes from percussion, not the frequency of muscle motion. Now, if they kept their foot in contact with the ground and jiggled it to induce seismic waves at the muscle frequency, that would count.  But even elephants don't do that; they still use air as an intermediary to generate sound waves that couple to the ground.

Bees.
Research has been done into their waggle dance. Bearing in mind that inside the hive there are very low light levels, and that only  a certain number of bees can be in direct physical contact with a bee at any given time.
The "waggle" of the abdomen occurs at between 12-15 Hertz and is modulated as part of the communication. The peculiar thing is, the sound is quite directional, and at the head, the pressure changes are at a minimum - indicating to nearby bees the direction at that point in the dance, and the direction and amplitude of maneuvers expressed.
The wing beats are pulsed at 20 ms duration at frequencies ranging between 200-300 Hz. These generate near-field sound which is heard by others, detected by the second segment of their antennae, and the sensilla (hairs found all over their bodies, though I'm not sure if it's known which are frequency-sensitive).
There is also my personal testimony:
My dad was an apiarist. When a bee gets angry and decides you're a threat, it releases pheromones which smell a bit like bananas.
When it gets really angry just before it stings, it buzzes a loud high-pitched whine with it's wings, while hovering near or just attached to it's target (me, often enough to not discount it as a one-off). I hypothesize that this gives a signal to nearby bees - more directional that pheromones which can swirl around objects with the breeze. Or maybe to scare the threat away. I'm darned if I can find reference to this phenomenon on-line.


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Free diving physiological changes
When training for free diving, there are several physiological and psychological changes that enable this activity, however one of the changes that I do not understand is increased resistance to blood acidification.
Part of the resistance to pain is psychological but from my understanding the body itself is also less sensitive to the carbon dioxide buildup in the blood itself, so I am wondering how this happens. Is this a change in the nervous system, blood or chemoreceptors themselves?

According to Libretexts Medicine link There are two types of chemoreceptors that help regulate breathing. Those with the most impact, the central chemoreceptors, can be desensitized. The relevant quote is:

Central chemoreceptors: These are located on the ventrolateral surface of medulla oblongata and detect changes in the pH of spinal fluid. They can be desensitized over time from chronic hypoxia (oxygen deficiency) and increased carbon dioxide.
Peripheral chemoreceptors: These include the aortic body, which detects changes in blood oxygen and carbon dioxide, but not pH, and the carotid body which detects all three. They do not desensitize, and have less of an impact on the respiratory rate compared to the central chemoreceptors.

From FreediveUK website. There are two types of breath training necessary. One is psychological, to learn to control the breathing reflex due to high CO2 levels and the other is to train the body to operate with lower levels of O2. They also mention the mammalian dive reflex which produces a physiological response:
When the face is submerged and water fills the nostrils, sensory receptors sensitive to wetness within the nasal cavity and other areas of the face supplied by the fifth (V) cranial nerve (the trigeminal nerve) relay the information to the brain.1 The tenth (X) cranial nerve, (the vagus nerve) – part of the autonomic nervous system – then produces bradycardia and other neural pathways elicit peripheral vasoconstriction, restricting blood from limbs and all organs to preserve blood and oxygen for the heart and the brain (and lungs), concentrating flow in a heart–brain circuit and allowing the animal to conserve oxygen.

As an aside: If you go to the freediveuk website they have an article warning about using hyperventilation. You would think this would help, and it was actually taught for many years as a technique. But it turns out that this greatly lowers the concentration of CO2 and you do need a high level of CO2 to signal that it's time to surface. What can happen is that the diver stays down too long, so uses too much O2 and as the diver gets close to the surface the O2 partial pressure decreases and the O2 level in the blood falls so low that the diver blacks out.


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How do we see the violet color?
Here is exactly the same question with an accepted answer. However, that answer looks wrong (I can’t find the “alert moderators” button). Firstly, it refers to a dubious source. Secondly, it contradicts this answer, which states that L cones do not have increased sensitivity in the violet area. This is also evident from the pictures on Wikipedia [1] [2].
The question is further complicated by this source. In it, the relative sensitivities of the M and L cones are exactly the same for violet.

How do we distinguish the color violet from blue? If a source of monochromatic deep red color is added to a source of monochromatic far blue color, will the effect be equivalent to the violet color?

Does the answer at https://biology.stackexchange.com/questions/51870/can-red-cone-cells-actually-see-much-red-light help?

Or https://biology.stackexchange.com/questions/26216/advantage-of-opponent-color

Or note that while "the relative sensitivities of the M and L cones are exactly the same for violet" may be true, this is not true for blue, and that's how you tell them apart.

Links are useful and I agree with the assumption. But here https://biology.stackexchange.com/a/85105/80210 the adopted answer with a positive rating contradicts this.

Okay; this isn't a very good place to complain about that. 4 users including the question asker found it useful, that's what the "rating" means. Other commenters have also pointed out an issue with it. Note that various plots of "cone sensitivity" come with different assumptions: with the eye or in a dish, for example, so you wouldn't expect them to all look the same.

Another related question: https://biology.stackexchange.com/questions/56385/how-are-colors-outside-the-standard-rgb-color-scheme-perceived

The fact that an accepted answer is incorrect does not justify reposting the same question. Acceptance is in the gift of the original poster — it doesn’t mean the answer is correct. Upvotes for an incorrect answer are annoying, but a limitation of the SE model. All you can do is downvote the accepted answer and explain why it is incorrect. To bring it to the list attention, provide an answer yourself, or perform a minor edit on the question (add or remove a tag, if you have the privilege or ask one of us).

Does this answer your question? What is violet color?

That answer looks wrong. It refers to a dubious source beause L cones do not have increased sensitivity in the violet area.

Color perception: There are several competing/complementary theories of color perception: the most popular, trichromatic theory, being complemented by the opponent process theory. There is also Land’s Retinex theory and Goethe’s (yes, that Goethe) Theory of Colors.
According to Peter Vishton: (Teaching Company, Secrets of Human Perception)
Overall, the opponent process theory of color complements the
trichromatic theory of color. The trichromatic theory explains the
retinal receptor level, whereas the opponent process theory explains
processing in the lateral geniculate nucleus and the visual cortex
The perception of color by the human brain is an extremely complex interplay of many functions of which the frequency and intensity of light entering the eye is only one. (Do you remember The Dress)   Color is an artifact manufactured by the brain. How the brain interprets color depends on, amongst other things, the ambient light, surroundings, shadow and contrast.  A white table cloth appears white when illuminated by daylight, but also when illuminated by a yellow light for example a candle.
Edwin Land (of Polaroid fame) performed many experiments: Land
In one set of experiments, the illumination was adjusted so that, for example, a white area of one Mondrian sent to the eye exactly the same triplet of radiant energies as a green area of another Mondrian. The two areas continued to appear white and green. Retinex Theory
However, to answer your question from trichromatic theory:
The receptors send a series of impulse to the brain proportional to their response to the frequency and intensity of the light striking them. The brain interprets the color it sees by comparing the levels of response from the various receptors. Different relative levels are interpreted as different colors. So, from your diagram S=10%, M=0.5%, L=0.5% activation is interpreted as violet. Rods will give a measure of the total intensity of light for comparison.

If you consider the sensitivity of the different receptors to violet light, the output from these is a unique combination that is sent to the visual cortex. There is no other possible light source that will produce this array. The brain has no trouble labeling this as violet.
Blue light would send S=100%, M=10%, L=5%    (This assuming log10 scale)
Adding blue light to red will give magenta - for which there is no single monochromatic color.

I refer to the comment of Bryan Krause and the data you provided:
If the M and L cones respond similarly for violet, and dissimilarly for blue, then that is a simple explanation for how you tell them apart.

Ryan Unfortunately that statement is also true for green (550nanometers) although the blue S is much less intense.

Your answer is excellent, Rich, especially in explicitly naming trichromatic theory. Besides upvoting it myself I don't have much more to do here; this answer was never developed properly, and was just drawing attention to a comment


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Portal hypertension
"Portal hypertension is more frequent and manifests in more complex ways in chronic liver failure than in acute liver failure (Fig. 14.7). It stems from increased vascular resistance coupled with increased portal blood flow. The increased resistance to portal flow is at the level of the sinusoids and is caused by contraction of vascular smooth muscle cells and myofibroblasts, and disruption of blood flow by scarring and the formation of parenchymal nodules. Increase in portal venous blood flow is due to arterial vasodilation. The increased splanchnic arterial blood flow in turn leads to increased venous efflux into the portal venous system." Robbins & Kumar Basic Pathology.
In liver cirrhosis, the blood neither from the hepatic artery nor from the portal vein are able to enter the liver normally, hence blood backs up in both, right? With the following: "Increase in portal venous blood flow is due to arterial vasodilation", how does the arterial vasodilation cause an increase in portal venous blood flow? Which arteries is it talking about? If for example the hepatic arteries are in vasodilation, more blood fits them hence less blood would go into the portal venous system, so how would there be an increase in the portal venous blood flow? Am I simply missing the picture of the circulatory system around the liver?
Moreover, with "The increased splanchnic arterial blood flow in turn leads to increased venous efflux into the portal venous system", why did the splanchnic arterial blood flow increase? Venous efflux from where and why into the portal venous system?
Many thanks for any help!

Splanchnic refers to all the abdominal cavity organs, not just the liver.
The portal vein system carries blood from these organs to the liver instead of directly back to the heart. The more blood flows to these organs, the more goes through the portal system. Vasodilation increases blood flow because there is less resistance when the vessels are wider.
This is all a compensatory mechanism gone a bit wild; there's not enough flow through the portal system. Normally, arterial tone sets flow, so normally if there's not enough flow it's because the arteries need to relax. As they relax it does increase flow, but because it isn't actually the arteries that are the problem (the problem is the pathology in the liver) there is even more hypertension in the portal system.
Remember, too, that veins are low-pressure vessels. Hypertension in the veins is a problem at much lower pressures than normal pressure in the arteries.

thanks so much for your answer! What causes the relaxation of the arteries? Something released by the cirrhotic liver? And which arteries are in question?

@DritaRaci The splanchnic arterioles: small vessels throughout the organs of the gut. I don't know what specific vasodilators cause the relaxation, I don't think it's any one specific molecule; it's not from the liver directly it's part of the compensation for reduced blood flow.

You want to take a whole-systems approach here. When blood isn't flowing well through the liver, that affects blood flow everywhere upstream too. The total flow in a cross-section through the vasculature is equal. So if you aren't getting flow through the portal system, you're also not getting flow through the veins feeding it, through the capillaries in the other organs that the portal flow comes from, through the arterioles that feed them, etc. This creates local signals that say "hey, I'm not getting enough oxygen/blood" and that makes the arterioles dilate to let more flow in.

Same thing that happens when, say, muscles are active and using more oxygen.


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Why would decreased temperature be associated with increased cell size, in deep-sea crustaceans (or in general?)
I was reading Wikipedia regarding deep-sea gigantism -- the fact that deep-sea species are often much larger than their shallow-dwelling counterparts. The article said,

Decreasing temperature is thought to result in increased cell size and
increased life span... both of which lead to an increase in maximum
body size.

The citation is:
S F Timofeev Izv Akad Nauk Ser Biol. 2001 Nov-Dec:(6):764-8.
[Bergmann's principle and deep-water gigantism in marine crustaceans]
I haven't tried to retrieve that article because I can't read Russian. Following up on "Bergmann's principle" doesn't help; it's just identifying ecographic patterns in gigantism.
From a surface area to volume ratio perspective, I can see how smaller cells are adaptive to cold temperatures. A huge amount of cellular processes are diffusion-driven. All of them, except for some potential electron or proton tunnelling processes, all mediated with thermal movements.
So let's say the transport of glucose into a given cell is driven by the concentration gradient (diffusion). At lower temperatures the diffusion rate is lower, so a cell of a given volume gets a reduced import of glucose. So it seems that increased surface-to-volume ratio (a smaller volume) would allow for a cell to compensate, and to accomplish the same rate of import as the warmer cell. This would also apply to some intracellular processes.
So assuming my thinking about diffusion processes is irrelevant to the real-life biology, as it predicts for colder temperatures that smaller cells are adaptive, is the point that metabolic processes are slower at lower temperatures? Then, a reduced rate of transport is not necessarily the limiting factor. Maybe the cellular volume can be scaled up until the total metabolic flux is comparable to the warmer-living cell? If there's more dissolved oxygen at lower temperatures, and if oxygen equilibrates well-enough, maybe no other nutrient or signalling diffusion is relevant?
This thinking does not at all seem consonant with this story by Curtis Deutsch and coworkers: Impact of warming on aquatic body sizes explained by metabolic scaling from microbes to macrofauna.

The model reproduces three key aspects of the observed patterns of
intergenerational size reductions measured in laboratory warming
experiments of diverse aquatic ectotherms (i.e., the "temperature-size
rule" [TSR]). First, the interspecific mean and variability of the TSR
is predicted from species' temperature sensitivities of hypoxia
tolerance, whose nonlinearity with temperature also explains the
second TSR pattern-its amplification as temperatures rise. Third, as
body size increases across the tree of life, the impact of growth on
O2 demand declines while its benefit to O2 supply rises, decreasing
the size dependence of hypoxia tolerance and requiring larger animals
to contract by a larger fraction to compensate for a thermally driven
rise in metabolism. Together our results support O2 limitation as the
mechanism underlying the TSR, and they provide a physiological basis
for projecting ectotherm body size responses to climate change from
microbes to macrofauna.

are there any deep sea animals limited by a skeleton or exoskeloton? that wouldn't be related to cell size.  another consideration is whether the cell size difference is average or median.  I know there are a few single celled organisms that are like the size of the basketball that live on the sea floor. most of the sea floor is deep, so if you have a few species down there like that, they could dramatically increase the "average" cell size without affecting the median. then again, maybe Caulerpa taxifolia is proof that actually the largest average cell size is actually not in the deep sea.

I didn't know about how large the cells can be in C. taxifolia. That does seem to place tensions on any theory that emphasizes deep sea conditions and doesn't include oxygen availability as a factor. Since photosynthesizers generate their own local oxygen, they would be able to flaunt any biophysical constraints on cell size for ectotherms mentioned below in @Eonema's answer.

Woods (1999) proposed an explanation for the negative effect of temperature on ectotherm cell size based on the rates of transport and metabolism of oxygen - both of which you considered in your question. The diffusion of oxygen decreases with increasing temperature. However, this effect is small compared to how much the consumption of oxygen increases with increasing temperature. Therefore, in a warmer environment, despite having greater oxygen supply, a cell is still more oxygen-limited because of the relatively greater increase in the oxygen demand. In a colder environment, a cell can be larger because it is less oxygen-limited and can afford to have a lower surface area:volume ratio. As Woods puts it:

The critical observation is that oxygen supply (determined jointly by [the surface concentration and diffusion coefficient]) rises slowly with temperature, but that oxygen consumption rises rapidly with temperature. Thus, at higher temperatures, the oxygen gradient within a metabolizing sphere will be steeper, and the radius at which the oxygen concentration at the center falls to zero will be smaller.

Note that while this hypothesis makes theoretical sense, it's not clear that the effect of temperature on cell size actually drives differences in body size or even occurs in nature. The study on temperature and cell size (Van Voorhies, 1996) that was cited by the Timofeev (2001) paper was solidly refuted by Partridge and Coyne (1996) for looking at genetically identical individuals and failing to consider latitudinal genetic variation, along with other sources of faulty inference. There are a number of plausible competing hypotheses to explain deep-sea gigantism and Bergmann's rule, not all relating to cell size.
Nevertheless, this same process proposed by Woods could also apply to organisms as a whole, rather than individual cells. Deutsch et al. (2022) consider the same mechanism as Woods, except they considered whole organisms. Therefore, their equations are somewhat abstracted from the biophysical processes that Woods deals with, but it's basically the same mechanism.

Bergmann's Rule is ecographic, but that's because higher latitudes tend to have lower temperatures. "The rule derives from the relationship between size in linear dimensions meaning that both height and volume will increase in colder environments" from the wiki article.

First, some corrections to assumptions in your question. As I pointed out in my comment; Bergmann's Rule is ecographic, but that's because higher latitudes tend to have lower temperatures. "The rule derives from the relationship between size in linear dimensions meaning that both height and volume will increase in colder environments."
Also a careful reading shows that rather than contradicting you, Deutsch and his collaborators’ article fully supports your hypothesis; “Maybe the cellular volume can be scaled up until the total metabolic flux is comparable to the warmer-living cell?” Not only that but increasing temperature increases the metabolic rate, further exacerbating the problem of oxygen uptake for the warmer cell.  From the Woods article quoted by Eonema: “rates of reaction are more sensitive to temperature than are physical processes such as diffusion and electrical conductivity.” And Eonema correctly states that in larger cells this increased rate of metabolism prevents the diffusion of sufficient oxygen to the center of such cells.
From the Deutsch article; “Among aquatic ectotherms, the TSR has been ascribed to limitation by dissolved O2. According to this hypothesis, a thermally driven increase in O2 demand outpaces any rise in O2 supply, a balance that can be restored by confining growth to a smaller size, resulting in a larger ratio of respiratory surface area to body volume.”
And from your excerpt:
“Third, as body size increases across the tree of life, the impact of growth on O2 demand declines while its benefit to O2 supply rises, decreasing the size dependence of hypoxia tolerance and requiring larger animals to contract by a larger fraction to compensate for a thermally driven rise in metabolism.”
The Deutsch full article shows that it is the oxygen concentration decreasing with increasing temperature, rather than the temperature increase itself,  that is the real driver of TSR.
The paper introduces several different models and experimental results to compare the effects of increasing temperature and decreasing oxygen concentration across a wide range of fauna, from bacteria on up.

This relates resting oxygen demand rate to size.
Whilst the Deutsch paper does not directly address increasing cell size, it does show the same effect in bacteria and other microbes, indicating that this probably applies to individual cells in larger ectotherms.
So, in conclusion, it is the decreased metabolic rate, coupled with the higher oxygen concentration in cold water that enables and encourages larger cell and animal sizes.
This answer has not addressed the possibility of longer lifetimes on increased size.

Besides the assumption that my considerations of temperature-dependent metabolism were different from the model of Deutsch and others (thanks for explaining how my picture is closer to theirs than I thought), what assumptions needed correction? I wasn't saying anything about Bergmann's Rule (other than correctly labelling it as ecographic). My question is focusing entirely on deep sea gigantism and the role of low temperatures in supporting it on a cellular level.

It was just that you said " Following up on "Bergmann's principle" doesn't help; it's just identifying ecographic patterns in gigantism." I was only pointing out that Timofeev's paper refers to Bergmann's principle as related to temperature rather than location.  "An increase in the geographic latitude and depth of crustaceans habitat (correlating mainly with lower temperatures) leads to an increased cell size"


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What effect does L-cysteine have in a growth medium on Lactobacillus and Bombilactobacillus found in bee species?
To cultivate Lactobacillus and Bombilactobacillus species we used MRS supplemented with 2% fructose in both aerobic and anaerobic conditions and also MRS supplemented with 2% fructose and 0.1% L-cysteine. The second medium showed significantly better growth in both conditions therefore we attributed this effect to L-cysteine. Could anyone explain why exactly this would have made a difference?

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