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If the Brain can store as much information as a billion hard disks why cant i memorize a single word document of random letters?
I read a lot of articles on this and all seem to agree that the brain storage in neural connections is tremendous but that doesnt explain why we forget things so easily and have such a modest memory in our subjective lives and we use much humbler devices to store information, i specifically wanna know if we can really store this information but the problem is we cant acces them as efficiently as a computer can or the whole process of storing this information is different than a hard disk on a computer.
None of the articles i have read make any comments addressing this question.
Links to relevant information on memory processing and storage will be appreciated.

I think your question is based on a false premise. How do you know you can't? Have you tried? People can memorize apparently random information e.g. >10⁵ digits of pi ...

Some people can but the statistics is of the regular human brain what stopping everyone from doing that(and 10^5 is also almost nothing compared to a computer storage)

The brain is trained to remember patterns and predictable associations. Randomness is the absence of patterns, so it's the exact opposite of what the human brain is for. A human can remember random numbers to about 67,890, which is the world record digits of Pi. That's about 20 pages of irrational numbers. Some people can remember 20 pages of word documents.
To memorize random numbers, the brain has to join colors, places, objects, people, animals, onto the randomness and construct a story to which the randomness can correspond to. It gives an idea of what the human brain is very good at memorizing, which is real-world phenomena through experience.
The human brain actually predicts what it has seen before it knows: It represents an expected object, personality or event from imagination (for example if you see a rabbit/cat beside the road and it turns out to be a bag). New objects like a page of random letters are compared to previous patterns of sensory input.
There are regions of the brain which are especially designed for tesks which are more like computer-memory, especially the task of geographic memory used for path-finding, food sources, which is called the hippocampi, which taxi drivers have very developed.
A computer actually uses man-made tools to do the memorization. A computer can't design a hard disk or a memory module, the computer uses human memorization tools, which humans can use too if you change the rules of the game a bit... they can use pen and paper... in that sense humans and computers are equal, with the computers being subservient to the humans.

Our brains usually make associations to different words including images, sounds, emotions, etc... which help reinforce the neurological patterns required to memorize sentences, etc...
To remember something, it must also be repeatedly 're-thought' to strengthen the memory. Eventually with enough conscious and subconscious repetition of a thought, these neural networks for that memory will move to the hippocampus where long term memory is stored.
memorizing 'random letters' doesn't seem to have much of a use. Making connections to these different letters will help give them meaning that your brain can hold on to allowing you to hopefully (with enough practice) memorize the whol word document.
There are however people (some considered savants) who have an ability called hyperthymesia which forces them to be able to remember everything that they have experienced in their lives.
This article: https://www.psychologytoday.com/us/blog/defining-memories/201706/why-we-forget discusses in great detail why we forget and I strongly suggest you read it (I find it very interesting).

I'd just like to add that, in addition to what has already been said, it can be a lot harder for the brain to memorize information that it doesn't find useful or relevant. As someone with ADHD, this is a common issue for me. I find it significantly more difficult to not just pay attention to, but remember information on topics that I don't find intellectually stimulating. I believe this has in large part to do with the way my brain filters out information that it deems unnecessary to remember. After all, why waste precious mental storage space on a word document of random letters? It is still possible to commit that kind of arbitrary information to memory, though, as we've seen from people who've managed to memorize thousands of digits of pi, but that takes a lot of practice and dedication, as the human brain was never really designed for such a task.


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Why do many humans, including myself, find cats so cute?
After all, they are descendants of big, dangerous lions and other wild cats, which doubtlessly have eaten many humans in the past, and probably continue to do so in some places even today.
Yet we for some reason find these tame, small versions of the "real deal" very cute. Even though they are still usually very arrogant, selfish, sadistic and whatnot, even when not physically posing a threat to humans.
Actually, I find even lions and leopards and pumas and cheetahs and tigers to look "cute", even though I wouldn't try to pet one for obvious reasons. I like the idea of truly dangerous cats not eating me and acting like "guard cats", but I wouldn't risk it even though there have been such cases where a human got accepted by lions who could kill him in an instant, yet don't.
I hate "eight-legged freaks" (spiders), yet I cuddle all the time with a four-legged beast which is much bigger. I would never stop washing my hands if I ever so much as touched a spider, but I can drill in my face into the fur of my cat and can't get enough of petting him and giving him expensive cat food and letting him in and out from the balcony door, etc.
It doesn't make sense to me. What is it about these furry animals with tails that is so appealing to many of us? It seems so natural for there to be a fluffy cat in here, sleeping/relaxing most of the time, but really, it's just a slightly-less-wild mini version of a lion, and who knows what he'd actually do if he were "full-size"? Probably eat me for closing the kitchen door on him...

Cute?  "…three proper Men out of five will always throw things at a Cat whenever they meet him" Rudyard Kipling.

You might turn the question around, and ask why you (and many other humans) have an irrational dislike of "eight-legged freaks" :-)

It's a very good and interesting question in general, but it's a difficult fit as a Stack Exchange question. It is possible that a more scientifically-written version of this question might be on-topic in Psychology & Neuroscience SE It can probably be on-topic here as well but it only takes five cat-dislikers to close it (humor).

@jamesqf or why cats have irrational dislike of cucumbers and skinny eggplants (search YouTube) (random example)

Cuteness is a subjective term to designate a psychological response to neotenic features (i.e. features that delay or slow in their growth) of the body mostly associated with young animals. These are features where the body parts are proportionally exaggerated compared to other body parts and the adult stage. It make the young individual attractive to the human observer - and most likely to animal observers as well - which is the psychological response. This response is an evolutionary adaption to assist in caring for offspring by inciting nurturing behavior in the parent(s), a hypothesis first proposed by Konrad Lorenz (1943, 1 ; but see also 2). Since other animals display neoteny, the physiological response can be transspecific (i.e. across species).

I like your answer very much. Care to add a reference to better complete your answer? I think this one actually testing Lorentz's idea of Kindchenschema ought to suffice! And as a bonus I suggest explaining the jargon terms (neoteny and transspecific) so that laypersons can understand the entirety of what you put so well. Those are very alien words to non-specialists.

@ S Pr, thanks! I hope sufficiently honored your request.

No, thank you. Good work :)

some recent research has hypothesized that felines, especially cats, evolved cuteness. Cats, unlike other animals domesticated themselves. Crescent, wild cats adapted to living with humans, hunting rodents in grain stores and abandoning their aggressive wild-born behaviors, which led to today's house cats. Also according to another research, the more something resembles a human baby, the cuter we think it is. It’s believed that when an animal has the same dimensions and features of a baby, it hijacks a neurological response to care and protect the creature. Moreover, the way kittens meow at us, it is very similar to how a human infant might cry. They modify their sound when seeking food, adding a higher-frequency element that exploits our sensitivity to infant wails and thus making it harder to ignore.

This doesn't really explain why many humans also find many other furry animals, especially young ones, to be "cute".  Sure, dogs might likewise have evolved (or been bred for) "cuteness", but this doesn't explain horses, ferrets, lambs & kids (that is, young goats), even bear cubs.  Indeed, the fur-cuteness link has sometimes caused me to wonder how human infants manage to survive.  Poor little things, having to go through life with no fur, no tail, no floppy ears... :-)

This is very interesting. I think you should add the citation to the research.

source: Stack Exchange

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sort: votes


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Why do some plants develop a shiny layer that looks like plastic?
I noticed some plants that look almost as if they were made of plastic and am wondering what and why that is. Here is a sample photo:

My guess is that this might be some sort of waxy cuticle that protects the plant from either water loss or pests.

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How do big cats perceive objects, specifically vehicles?
Right so we have been on safari in South Africa recently and before encountering big cats (lions) we have been told to hold still and not reach out beyond the boundaries of our safari vehicle because the cats would see it as uninteresting "object", unless something sticks out or moves.
Having a bit of background in biology I tried to map this to a more "scientific" explanation but wasn't successful so far. How would you describe the cognitve perception of vehicles by big cats (or lions specifically)?

It's basically the same as humans, they include higher predatory associations and less logical and word associations. The neural circuits study all the images received from the eye and compare new objects to previously learnt categories: Bird/Log/Horn/flailing upside down limb/face/car/rhino... You can feel your own neural networks at work when you focus on an unidentified detail (bird/branch/rock) and class them into right and wrong results. Moving objects occupy a moving class of their own, i.e. in your garden, they are a potential threat or a prey.
When the truck is rolling along normally, the cat has extensively studied this kind of object already and has made these associations: Glass windows he can't get into, faces inside glasses, rubber tires, slight smell of humans, major smell of petrol and artificial stuff, indestructible, square and round bits, sees it every day from all angles and has interacted with trucks plenty of times. He rarely gets any food from safari trucks, they all look a bit the same. A truck occupy the same prey opportunity as birds in trees which can just fly away.
The brain behaves differently towards known objects and movements and new, unknown animate objects, the unknown animate things result in: the capture of attention.
When there is an arm waving out of the window, the cat's brain is receiving an unidentified living thing attached to the truck, perhaps some kind of living meat! A living thing, a prey. Is it a leg of lamb? is it inside or behind the box? Can he get into this truck? Is it a bird? The cat will be interested in the unidentified, new kind of living thing until he has figured it out.
general reading.
visual cortex of monkeys and cats.
Activation of the hypothalamic feeding centre upon visual prey detection
other research.

Any animal may see something moving in its territory as a challenge.  Big cats and other predators are very intelligent and have an excellent sense of smell. Just because you're not sticking your arm out, doesn't mean that they don't know you are in there.  Lions are basically lazy and will rarely attack people in a car, but it would depend on the animal's prior experience with other vehicles. If they have been harassed or fed by tourists trying to get a photo, big cats (and other predators like bears) are more likely to approach a car. I have seen cheetahs and leopards jump through an open window into a Jeep.  You can watch this video or search youtube.com for others.  https://www.youtube.com/watch?v=-LFTJ-BFWms
Hippos, elephants and rhinos have attacked cars for no apparent reason, especially during breeding season.  Best advice? Stay in the car with your windows all the way up!

Right - that's exactly what you hear when talking to guides etc. I am interested in the scientific answer to why? Is being lazy the real reason for lions etc not showing interest people in cars? And btw. windows up is a nice advice - most safari vehicles are complete open...


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What determines whether a trait brought out through sexual selection is transmitted only to offspring of the same sex or of both sexes?
First of all, let me apologize for my amateurishness. I have no background in biology. Please bear with me.
My question relates to sexual selection, or specifically its most prominent manifestations:

competition among males which is resolved through male conflict
competition among males which is resolved through female decision

Let us postulate the traits that these two forms of selection might bring about, e.g., strength for the former case and attractiveness for the latter. Of course this may vary. Would I be right to say that whether this trait is passed on through the Y chromosome or whether is it passed on somewhere else (and therefore to both male and female offspring) is a question of probability? If so, what do the odds look like?
The aim of my question is really to understand how selection among men has changed the human species in general. It is well-known that aggression, charm, and paternal care are some traits that have evolved among men. But how would we go about measuring the impact of this selection upon the gene pool of the entire species?
Lastly, is there any literature based on evolutionary research that concerns my question in particular?

check out Monoamine Oxidase 1 (MOA1) gene. Very complex question to answer, there are a huge number of factors including things like hormone expression.

Whoops - MAO gene - apparently called MAOA, not sure where I got the 1 from.


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How does the blood flow in the glomerulus when everything except plasma is drained out?
So I learned that in the glomerulus, everything smaller than the RBCs is filtered out, but I had learned previously that - Blood needs plasma, water medium to flow. So if its drained out into the Bowman's Capsule, how does the blood leave the efferent arteriole.
Could anyone please clarify,
Thank you.

Welcome to Biology.SE. I'm almost certain that you are misreading (or reading from a source that is in error). Please check this 'fact' with additional sources and then (if this astounding claim is true) update your question to include supporting references to reliable sources (preferably primary literature, but textbooks are acceptable if they are available online). If this is based on someone's misunderstanding/miswriting then please delete your post.

If it were true (and this is but one small example in the scheme of things) protein, lipids/lipoproteins, and glucose in the urine would be of absolutely no concern.

Pardon me for my ignorance. So what actually happens? It wasn't explained clearly in my textbooks or on the internet.


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Cannot seem to merge the two circles of a microscope (biological, binocular)
I have recently purchased a binocular microscope (Saxon Researcher Compact Biological Microscope 40x-1600x), and have had difficulty getting the two circles of light that I'm seeing through the eyepieces to merge. I've focused the microscope without much difficulty, but when I look through I still see the two circles. Researching this problem told me to bring the eyepieces closer together until the circles merge, however when I do this, I just stop seeing through one of the eyepieces (I close one eye, nothing changes, I close the other - and I just see black in the eyepiece. Also when I move my head slightly I can see through the other eyepiece, but as soon as it's adjusted so I can see through both there's the two circles ). Does anybody have any suggestions as to how I could fix this?
Additionally in my research I saw that you eyes should be 1.5-2cm from the eyepieces, but I cannot see anything but a small dot in the centre until my eyes are almost pressed up against the lenses, is this wrong?

One problem seems to be a small "exit pupal" typical of inexpensive equipment. It is the size of the circle you see in the eyepiece.

Your best bet is to measure your inter-pupillary distance and use this to set the lenses at the correct distance on the scale on the centre piece between the eyepieces. The black indicates that you have something mis-aligned, probably the eye-pieces are raised or lowered with respect to each other, rather than equally adjusted about a central point. It may also be that you have the dioptre incorrectly adjusted so one lens is a lot closer to you than the other.
To measure your inter-pupillary distance you need a ruler (marked in mm preferably, as this is the standard for most microscope inter-pupillary distance scales) and a mirror (or alternatively someone to do the measurement for you).
Stand about 15-20 cm (6-8") from the mirror. Close one eye. Align the 0 mark on the mirror with the centre of one pupil, look straight ahead, close the open eye and open the closed eye, and measure the distance to the centre of the now opened pupil.
Now, you should be able to set this on the microscope. Once you have done this, test to see if you can see with both eyes. If now, adjust BOTH eyepieces equally in small amounts.
As for the viewing distance. To be honest I had never measured how far away my eyes are when using a microscope, but having checked, mine are about the width of my index finger away from the lenses. This would be about 1.5 cm, but not much further than that. In your case I would put my eyes close to the lens and slowly move away to a point that feels comfortable and that the light almost fills your field-of-vision.


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Measuring innate caring about offspring and long term surivavability
I am not a biologist, and don't have much technical knowledge of biology.
That being said, having observed the real world, it seems that, at least for mammals, human beings seem to "care" more about their offspring than other mammals might. One reason, of course, is the fact that human babies/children require more assistance than other mammal babies.
Imagine, however, that at any given point in time, we can summarize the resources that a mammal needs as $X$. A fraction of that $X$, call it $x=F/X$ goes towards the children. This could be for human beings, the fraction of income devoted each period to the child, for lions the fraction of meat given to cubs etc.  If a species gives $x=0$, then trivially, the species dies out. If a species gives out $x=1$, the species might still die out because it can only donate resources for one period, and the infant may not be able to fend for itself next period.
If one were to plot this $x$ over time across species, it would necessarily decrease, as the infants become autonomous eventually.
Is there any empirical work that correlates such a measure of "devotion of resources" to long-term survival of the species? In other words, are those species that survive long term best able to calibrate this $x$ to an optimal one to maximize survivability?

Arguably, 100% of any animal's resources go to offspring or are intended to go to offspring (sometimes you get eaten too soon), it's just a matter of how exactly those resources are allocated to different phases of the offspring's life. A female mammal is going to give a lot more post-birth resources than most other animals, but it doesn't seem quite fair to discount the effort put into eggs by other females, even if no post-natal care is given. Many species give every ounce of energy they have left to make as many eggs as possible and die immediately after.

And, certainly, animals spend some of their own resources running, climbing, or flying about, so that doesn't go directly to offspring, but it's still an indirect cost of preparing to reproduce. Even males that don't seem to put as much direct resources into offspring put resources into competition with other males, locating mates, etc, which are all resources dedicated to ensuring their next generation.

Yes you are right @BryanKrause . I thought of this after watching videos of say, lions eating before their cubs, when both were hungry. But this makes sense according to what you say, as the lion's survival is more crucial to the propagation of the next generation than say, any particular cub's.

@BryanKrause - The first thing I thought of when I read this was a male (mountain goat/whatever antelope) headbutting so many other males that it dies before they do (more energy expenditure and less time for nutrition), but gets to sire more offspring. It's not just about food allocation.


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Why do spiders hang up dead bugs?
I used to think the reason we see a lot of dead bugs wrapped and hanging on spider webs was that they get caught by spiders and after the spiders are done with the bugs they leave them there. But I have had a few spiders trapped in a plastic bottle and that assumption no longer seems correct. I haven't found any articles online that sufficiently address this.
I notice that the spiders in the bottle actually actively work to make web to hang up dead bodies, even if the bodies are much larger than them in size and are not their prey. For instance, there was a pretty sizeable spider in the bottle when I trapped a few newcomers. The large spider had been dead in there for weeks. I was just too lazy to get its body out. The newcomer spiders were much smaller but they soon worked to wrap up the dead body of the large spider and hoist it so it didn't stay at the bottom. The same also happened with the body of a moth several times their size. House spiders in general don't attack other bugs that outsize them or even their own size because they only attack bugs they can pin down. So the moth died of natural causes in the bottle-starvation I assume, but its body was also hoisted. Why do they do that?

I think that spiders like organisation. It can also be that they hang up bodies that they don't feed on so they attract predators for those bodies that they can actually feed on.

Spiders can eat things much larger than themselves, one of the advantages of a liquid diet. even after a spider has fed on something a husk is left behind.

It seems they do that to save food for later, at least that is what this source suggests. Could also be a sanitary thing, if the bug is dead for some time. Please be nicer to the invertebrates around you!


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Quantifying Hydrophobicity from amino acid sequence
fourth-year undergrad here so any help is super appreciated! Also this is not something I am working on for a grade, so pls don't think I am just looking for someone to do my homework lol!
In a gist, the project I am currently working on requires me to compare the same proteins involved in the Calvin cycle from both an extremophile and a mesophile. Specifically, I am supposed to figure out if the extremophile (which lives in the Arctic) protein's are more hydrophobic than the mesophile. I am expected just to use in sillico/bioinformatic techniques to figure this out
So far, all I have done is run the amino acid sequences through various hydrophobicity scales so each residue is given a ranking of hydrophobicity, then calculated an average from that. Obviously, this has a lot of flaws and is not proving to be very effective
If anyone has any ideas of programs or methodologies that could produce more accurate results I would be so grateful! I have been going in circles with this for a while now
Thank-you!

Please explain what flaws you think the method you are currently using has and what you mean by "is not proving to be very effective". Effective in what? Do you just mean you can't find any differences? And it hardly seems that "getting more accurate results" can be your problem — why would you think the measures of hydrophobicity are inaccurate? And are you just averaging values of amino acids for each protein, or plotting values graphically across a whole protein, as is possible?

Perhaps try to see if the protein is expected to be embedded in a membrane? See if hydrophobic parts are clustered, or if there is a signal sequence giving hints.

I believe that the standard hydrophobicity measure is protein GRAVY.
However, as David comments, I don't see any particular reason to expect that its estimates would deviate from what you find by other means, as it's just taking the average across the protein rather than considering any other aspects of structure:

Protein GRAVY returns the GRAVY (grand average of hydropathy) value for the protein sequences you enter. The GRAVY value is calculated by adding the hydropathy value for each residue and dividing by the length of the sequence (Kyte and Doolittle; 1982).

There are more recent, more elaborate methods that quantify different features of hydrophobicity, but I don't imagine that your professors are asking for these somewhat less readily interpretable measures.


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What are the determinants of tumor metastasis
Under what conditions do tumors migrate? Is it due to hostile microenvironment conditions, drug application, mutations, or other causes? Are there any migration probability values (I am doing an in silico research) or equations to determine this?

There are a lot of mathematical approaches to understanding metastasis.  Review articles might be a good place to start.  The long and short of the biology of metastasis is it depends.  Tumors are highly variable, some metastasize easily and in particular ways, others do not.  It is a heavily studied area of medicine.  I will add that it is probably not a "hostile microenvironment" that encourages metastasis; it is probably better to think of the proximate causes rather than such ultimate causes.

You might also want to read about the epithelial-mesenchymal transition as an initiator of metastasis.

So here's a sort of review article that may help you https://people.maths.ox.ac.uk/maini/PKM%20publications/367.pdf .. and perhaps this one as well http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4626809/

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Where can I find SSR and/or SNPs that locate RC1 genes in Soybean?
Where should I look to find SSR and/or SNPs that locate RC1 genes in Soybean?

SoyBase has Illumina SoySNP50K iSelect BeadChip and they've identified soy SNVs. You could find them in dbSNP - identifiers starts with 'ss'.

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What fills the spaces between non-fused sacral vertebrae?
What is in between the sacral vertebrae before they are fused?
I have looked and found no specific descriptions. If it is simply cartilage, what type of cartilage?


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Is eradication of the Common Cold possible?
This is a thought experiment, but everywhere I've read seems to say that colds ALWAYS come from someone else. There's no mention of a cold arising in someone without it coming from another infected being.
So my question is, if everyone in the world stayed out of physical contact and air space with everyone else for 2 weeks (or until every cold virus would have completely disappeared), would all variations of the cold virus then be extinct leading to a world without colds?
Or is there somewhere else that colds can arise from?

@rg255 I disagree that this is not of interest to biologists. If eradication of other diseases can be done, then it is perfectly valid to theorise about the eradication of diseases such as the common cold.

You'd think there would be numbers of papers on this. I have two references but they're not great.  The answer is not really.  Many people carry cold viruses asymptomatically.  This can be either a natural immunity, or that their body has beaten it down but not entirely eliminated it.  Cold viruses do not survive long outside of the body as you stated.  The only way they've made it this far is some survive inside the body until they are spread to other people.  In essence we are the reservoir.  So you could isolate everyone for two weeks, but that won't cause a problem for the viruses that are just tagging along.  There may be other reservoir animals as well for many of the viruses.  But even those that only affect and are carried by humans would survive.
The group of cold viruses is just too varied and different to eliminate them.  Also the cost of such an effort would not really be justifiable given the typically mild symptoms.
Natural Reservoir


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Would tattoos be considered a phenotype?
I'm trying to understand how broad the definition of "phenotype" is. If someone gets a tattoo, would that tattoo be considered part of their phenotype?

The fact that the two posted answers disagree is maybe a good argument to say that the answer is not obvious and the post does not "lack research". I am upvoting.

Hereditary biology doesn't often extend to human artwork, so it's a moot point. Tattoos fall into the realms of social sciences / human sciences and they are not very useful for measuring genetics, which is what genotype and phenotype are aimed for.

Tattoos are not considered part of genetics, a scientific measure of genetic heredity, and no established science paper would quantify tattoos as an indicator of biological phenotype. Tattoos are anthropology, artwork, they would only be referenced as phenotype in a joke paper.

Standard definition of "phenotype"
The term phenotype is generally not clearly defined. Most often, textbooks will define a phenotype as any anatomical, morphological, physiological or behavioural observable characteristic of an individual. This definition is somewhat vague as it is unclear how far reaching the impact of the behaviour can be. To my knowledge, the only clear definition of a phenotype is its broadest definition as popularized in the book The Extended Phenotype.
The Extended Phenotype definition
In its broad definition, a phenotype is any manifestation in the world of the presence of a given genotype. I am unsure of the detailed presentation of this definition in the book but here is briefly my extended definition.
With the "extended definition", an individual phenotype is not limited to its body. Consider a bird nest as an example. In the "standard definition" only the bird building the nest has a phenotype, the nest itself in not part of that phenotype. With the "extended definition", the nest itself is part of the phenotype of the bird who built it.
With the "extended definition", an individual phenotype is not limited to its temporal existence. An individual can have much consequence to the world after its death. For example, the stoic philosophy of Marc-Aurel Caesar that has affected many people's life after his death is still part of Marc-Aurel Caesar's phenotype.
In short, imagine a world with and without an organism. The difference between these two worlds is the phenotype of that organism. Given the fantastic complexity and connectivity among events in the world, a lot of the world's properties can then be considered part of an individual phenotype.
Which definition is correct
Well, a definition is never correct or wrong. It is just a definition. But let's talk about clarity, uses and fit to theoretical models for both definitions.
Clarity
It is somewhat unclear what consequences of the genotype in the world are still included in the "standard definition" of phenotype. As such the "standard definition" is somewhat unclear.
Uses
For the vast majority of purpose authors use the term phenotype to refer to specific characteristics and therefore, the detailed definition does not matter.
Fitness of theoretical models
In theoretical work, the extended definition is the only definition that fully satisfy our models of ecology and evolution.
Phenotype and heritability
In a comment under the original post @Dirigible's said

No. Phenotypes are qualitative and quantitative characteristics that
arise from the interaction of an organism's genetics (genotype) and
the environment. There are no genetic determinants for tattoos. This
question lacks background research and I'm suggesting that it be
closed.

There might be confusion with the concepts of inheritance and of heritability here. Heritability of a given quantitative phenotype is the fraction of variance of this phenotype in the population that is explained by genetic variance (see this post for more info). If a phenotype (that has some non-zero variance) has no underlying genetic variance, then this phenotype is not heritable. But it still remain a phenotype.
By saying There are no genetic determinants for tattoos as a way to justify the No starting the comment, the comment sounds like (whether or not it was the poster's meaning) a phenotype is a phenotype only if it is heritable. I would strongly disagree with this claim.
More straight forward, @baca in his/her answer said
What would not be a phenotype is something that you could conclusively prove to have no genetics basis whatsoever.

Again, I disagree with this claim.
On top of that, I would argue that tattoos are very likely genetically determined. There are probably genetic determinants for liking tattoo. Probably for liking art in general. There are probably genetic determinants to joining gangs (such as loci affecting aggressiveness for example) that sometimes use tattoos as symbols of membership. There are skin conditions that prevent people from getting tattooed and some of these conditions are likely to be heritable.

@baca I think you are confusing the concept of "heritability" and the slightly undefined concept of "genetic basis" or "inheritence". Something can be "inherited" without being "heritable" (at least by the commonly used quantitative genetics definition of "heritable"). You might want to have a look at this post (already linked in my answer). Also, some phenotypic variants may be caused by environmental factors (e.g. getting bitten by a predator).

If a phenotype has to be heritable then infection can’t produce a phenotype.  Neither could stress. In the literature we normally call the behavioral responses to such things phenotypes.

I've made some mostly minor grammatical changes that I hope improve readability. ——— Comments: 1) Your answer seems to end abruptly mid-sentence — did something get cut off? 2) Can you provide references for "In theoretical work, the extended definition is the only definition that fully satisfy our models of ecology and evolution." 3) No one else posting here has used "heritable" or "heritability", so I think that part of your answer may not be relevant ...

I might have been a bit too quick to accept this answer, since there seems to be some debate about its validity, so I've unaccepted it for now. Depending on the results of the discussion and such, I will accept it again later.


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Is osmosis diffusion of water?
My textbook says this:

Osmosis is the diffusion of water.

Wikipedia says this:

The diffusion model of osmosis is rendered untenable by the fact that osmosis can drive water across a membrane toward a higher concentration of water.

It's my understanding that diffusion is passive transport, and it moves material from a highly concentrated area of that material to an area where it is in lower concentration. By this definition, it looks like Wikipedia is correct. But if for example, a cell is put in saltwater, water from within the cell would go out. Is this diffusion now? Which definition is correct?
I would just go with the Wikipedia definition because it actively describes its own definition as a refinement of the textbook definition, but the paragraph above in the article is a bit confusing to me.

Have you tried reading the sources at the end of the article?

This question is off-topic for Biology. It seems like you understand the process of osmosis, and are just curious if it's also a kind of diffusion. The answer to your question is either going to be based in physics or in the semantics of various definitions.

you will likely have better luck in the chemistry stack as this is only tangentially connected to biology.

Yes, In most cases, osmosis is the diffusion of water. To my understanding, what I think Wikipedia is trying to do is to assert the fact that osmosis is also be the movement of water from a region of lower water potential to a region of higher water potential. These kinds of contradictions, as much as scientists try to avoid them, still come to play because science is very complicated. Just when we start accepting a theory, it gets discarded by another theory.

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Osmosis is about solutions (solvent + solute).
Osmosis is a movement of the solvent through certain types of membranes. These membranes let the solvent move across them, but not the solute. The process tends to balance the solute concentration on both sides of the membranes.
If we say that the solvent is water and the solute is salt (NaCl). Water will move from the side of the membrane where the salt concentration is low toward the side where the salt concentration is high. At the end of the process both concentrations will be equal.
In biology it is a very important process at a cellular level (cell membranes are semi-permeable membranes) but also plays a key role in food digestion or kidney reabsorption, for instance. Cells (bacteria) that are put in solutions with high concentration of salt die of loosing the water they contain.

First, while this looks like it might be a good answer it is to a question that is off-topic for this site (because it isn't primarily a biology question) and it is better to leave such questions unanswered. Second, for future posts please note that answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Mithradates - Developing immunity to poison?

According to legend, Mithridates studiously researched and examined all known toxins and experimented with potential remedies by using prisoners as his guinea pigs. Supposedly, Mithridates’ toils paid off because numerous ancient authors, including Pliny the Elder, claimed that he created and regularly ingested a universal antidote for all identified toxins, and it became known as mithridate (mithridatium).

It was said that he was pretty much ingesting small amounts of poison to develop an immunity to it.
Whether universal poison or ingesting each type one by one, is this possible to build up your body to resist or be immune to poison/venom/toxins in general?

Hi mph85 and welcome to Bio.SE. I hate to be boring, but the answer is that it will depend on the specific compound. Perhaps you could narrow down the question to a specific poison?

May I remember you that Mithridates' body actually got tremendously marred from such treatment, (according to the same sources you have quoted).

Welcome to SE. Edit: The answer is in two parts based on the mechanism of action of the toxin. Courtesy: @David and @jamesqf
Immunity
The white blood cells in the body are responsible for recognizing self or non-self peptides and form the adaptive compartment of the immune system. The B lymphocytes have a receptor that can bind to various peptides. Upon recognition of foreign peptides in the body, they go through a reaction (somatic hypermutation) to become further specific to the foreign peptide. They also differentiate into Plasma cells which can now secret another protein (antibodies) which neutralizes the foreign peptide.
Small amounts, which are non-lethal, but in enough concentration to drive the B cell reaction creates an immunological "memory". This memory allows a faster response to the same peptide compared to the reaction. This in order allows the body to withstand a higher concentration of toxic peptide, which otherwise would have been lethal as its being neutralized.
Vaccines work on a principle very close to this.
Homeostasis
Every toxin interacts which some biological process and drives it out of balance. The body actively tries to restore the balance by some means.
For example, if a ligand is depleted the body can increase the number of receptors to counter the effect and vice versa.
By ingesting small amounts of toxins body can adjust the equilibrium by very small amount at a time adjusting the concentration of relevant ligands or receptors.
Again, the person who has been through this process can withstand a higher dosage of the toxin compared to a person who hasn't.

At least two problems with this answer: size of antigen and mode of presentation. Also, answers are answers to questions, not to people. This question is about immunity to poisons such as cyanide, arsenic, alpha-amanatin. Do you have any evidence that these can provoke an immune response?

@David I agree that it is dependent on the size of the antigen and mode of presentation to a certain extent. The last line in the description asks for a general possibility and I have only included details which I thought are relevant for the answer. OP also doesn't mention Cyanide, Arsenic, alpha-Amanatin specifically or any other particular category or toxins.

@Cheesebread: Or things to which you can become habituated, as for instance opiate addicts who can tolerate doses that would kill a naive user.  I've also read that one can develop a tolerance to arsenic (and perhaps other things) by taking gradually-increasing doses, to such an extent that suddenly stopping the dose will cause death.

@jamesqf — me too. Wasn't Rasputin supposed to have done that in relation to arsenic? But the point, then, is that this is nothing to do with lymphocyte-based immunity, so a good answer needs to consider the different situations.


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Does my nearsightedness come into play when creating light outlines in the distance?
After looking at a light and closing your eyes, you see an outline of the light. I was curious how my nearsightedness would come into play. I look at a light in the distance without my glasses on and close my eyes, would I be able to distinguish the light shape better than if directly looking at the light?

Welcome to Biology.SE! Since this is a question about your personal response to light is there something stopping you from testing this yourself? Note that we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

Not likely.  The afterimage you see when you close your eyes is an effect dependent upon which light-receiving cells in the retina (rods and cones) saw light when your eyes were open.  The blurry image you saw when your eyes were open has the same size and shape as the afterimage you see when you see when you close your eyes.  Because the afterimage has less detail, perhaps you would be less distracted by detail and be able to pay more attention to shape, but it seems unlikely that would noticeably help your idea of the shape.


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Why don't all my cell membranes "smush" when I fall?
I've read the question about cell membranes breaking apart, which is close to what I'm asking, though I'm trying to probe a bit deeper.
I understand that there are hydrophobic forces keeping the cell membrane together, and I'm roughly picturing the strength of something like water surface tension.  With this intuition, I tried to consider a few examples:

I've read the idea that the cytoskeleton can help give a cell structure.  But if a cell has some kinetic energy (say, red blood cells in the bloodstream) and runs into something else (say, the arterial wall), are the hydrophobic forces holding the cell membrane together strong enough to prevent the cytoskeleton from puncturing the membrane?
Similarly, there are videos of bacteria with their flagella traveling at what seem to be pretty significant speeds (relative to their size) - are hydrophobic forces truly enough to hold the cell membrane together in the face of that kinetic energy?  Are they a lot stronger than my intuition gives them credit for at the tiny scales of cells?
Hydrophobic forces also seem to require being in solution - the obvious counterexample would be our skin cells, which clearly are not fully in solution, but even if that were the case, if hydrophobic forces were the bulk of the forces, then wouldn't any two cells merge the moment they made physical contact with each other?

This train of thought leads to the titular question and thought experiment:
Dropping a glass of water will result in the water going everywhere.  If I were to jump up and then land, and hydrophobic forces are holding the cell membrane together, why doesn't my cell membrane fall apart from that application of kinetic energy?

The radius of an average human cell is approx $19$ micrometer. That gives it a a(n) (circular) area of $2000$ micrometer² (grossly exaggerating) = $2000 \times \left(\frac{1}{1000}\right)^2 = 0.00002$ cm²
If you fell on your buttocks on an area roughly $2$ palm spans, that would be an area of roughly $1000$ cm².
How many cells have you fallen on? $\frac{1000}{0.00002} = 50,000,000$ cells.
An average person weighs $68$ kg, that's around $680$ N. This force is distributed over $50,000,000$ cells. The force per cell (pressure) = $\frac{680}{50,000,000} = 0.0000136 \approx 10^{-5}$ Newtons. That ($10^{-5}$ Newtons) is the amount of force exerted by an object that weighs $1$ microgram. Pretty sure our cells can handle that amount of force.

One zero is omitted in 1/1000. In the final calculation it is repaired.

10^-5 N would be the weight of a 1 milligram object.

Pardon the error, errare humanum est.


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How to choose secondary Antibody?
when isotype of the Primary antibody is IgG2a (from Mouse) and IgG2b (from Rat), how to choose secondary Antibody against these Primary isotypes?
Does secondary Antibody is that much specific to detect IgG2a/2b? What is the logic behind choosing secondary antibodies? A detailed note in this regard will highly be appreciated.

Secondary antibodies go against species, so you would use something like goat anti-mouse. If you are using rat to label a different protein along with mouse, then you will need to use an anti-rat antibody with a different marker than the anti-mouse so that you can actually make the distinction.

You are not telling, what you do, but I think itis western blot - and for this application it is not important to know which isotype your antibody has. The secondary antibody (which is supposed to bind the primary) has to be directed against the isotype (IgG for example) and the species in which the primary antibody was made, in your case this would be this would be anti-mouse or anti-rat IgG. Since most commercially antibodies in the lab are IgG people usually don't think about it.
The reason is that the secondary antibody is directed against the Fc part of the primary antibody (which has a species specific sequence) and even with the differences in the sub-classes due to different assembly of the light and heavy chains this will not be detected by the secondaries. See the figure (from here) about the schematic differences:

With a careful selection of the peptides used for immunisation it is possible to generate secondary antibodies which can be used to distinguish between sub-classes.

Part of my job is developing ELISAs, and I use isotype- and subtype-specific secondaries all the time.

@MattDMo Adapted the answer. Maybe you want to write a more specific answer?


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How does the brain train its neural network?
One question that came up learning how artificial neural networks are working was how the brain can train its neural network?
When we say we have an artificial neural network, the problem behind it is a typical, but uncommon minimizing problem. The math behind it is logical and pretty easy. But it's math, so an computer can calculate it by doing millions of iterations. But the brain can't do that (I would be surprised)
So, how does the brain solve this task. Trial & Error, we don't know or is there an even more complex system behind it?
Thanks in advance.
GA

I'm voting to close this question as off-topic because it belongs on Cognitive Sciences S.E.

@AMR - not more on topic there than here. Wouldn't migrate. Wouldn't close here either.

@Christiaan This really isn't asking about a purely biological process. Sure you could talk about reinforcing neuronal connections through repeated usage and the underlying chemistry, but that doesn't get at the learning aspect, and I think that the mechanisms of learning are Cog Sci more than straight biology.

@AMR - good point. But CogSci often deals with it from a holistic perspective, while this question tends to aim at the network level. As such, given the low-level nature, it's ontopic on both ends from my pov

@Christiaan well, if you think there is an answer, then you are the expert. It just seems that also trying to make this relevant to the neural biochemistry of learning as well, may make the answer a tad long....

@AMR a close vote based on too broad would be perfectly acceptable to me for sure. I just wouldn't like to see this migrated.

this is one of the biggest open questions of the AGI field, a solution apparently nearly leads to AGI. there is some research trying to link gradient descent to brain neurology. also jeff hawkins postulates cortical columns are representing ML algorithms. Deepmind has some research relating to the hippocampus. may try to cook up some survey at some pt, but its an extremely challenging area to cite/ summarize current knowledge. the dopamine system has a lot to do with human rewards & presumably plays a large role. etc

The answer to this question is probably Hebbian Learning.
Hebbian learning can be nicely summarised with "Cells that fire together, wire together". So basically the synapses of neurons are strengthened if they fire in sync, and weakened otherwise.
One can easily see that a) this kind of local learning mechanism makes a lot more sense for the brain then some global method like gradient descent and b) this mechanism leads to stable representations of patterns.
In artificial neural networks this kind of learning is modelled in Hopfield networks and Restricted Boltzmann Machines.
Of course this simple rule barely scratches at the surface of what goes on in the human brain, when we are learning something. A complete picture would probably involve complex feedback mechanisms of inhibitory and excitatory connections between neurons, functional modules of neurons, and different parts of the brain.
But I fear these details are not yet well understood …

Oh. MY. GOD. I didn't through anybody would ever answer on this question anymore. :D Thx.


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Other than lignification how does secondary xylem attain its stiffness then balance that with remaining living processes?
I read in a textbook that the vascular cambium creates secondary xylem to its inside and outside. These cells, formerly conducting water, dry out and harden. Their cell walls get lignified creating wood, particularly in the cylinder between cork cambium and vascular cambium. This is actually three related questions.

Is a force exerted on the secondary xylem by the vascular cambium? A force that compresses these cells?

If "yes" to number one, how can soft tissues that make up the vascular cambium press so hard on the previous layers of harder (dried out) secondary xykem? Are concentric cylinders staggered so hardness increases gradually, with a stiffer already compressed cylinder exerting more force than newer secondary xylem cylinders?

The secondary xylem (cortex) is living. Medullary rays traverse them and it is adjacent to the living cork cambium. As lignin is deposited in its cell walls, what biochemical processes continue to occur? The hard walls would deter intercellular transport but the cells must continue interacting.

No i don't think cells harden because dividing cells apply force on them, if that was true I think it would make more sense for a tree to compress every time more an more as it divides in vascular cambium. What happensn is that it grows in diametar, I think only a few cells of that mass simply can't act on a much more massive body like that. A small ball will hardly move a big wall( given it is not travelling at speed of space shuttle:). Even if that was the case, I still don't see which force would be behing it, there is no gravity in lateral direction. If increasing diametar would provide more an more preassure on the inside than wider trees would have stiffer and stronger middle than tiny ones. And I don't think that is the case.

I am not an expert in botany, this is only my logic.

I couldn't understand how soft tissue would exert such a pressure either.

That leaves the other questions: what hardens the xylem other than lignin? The cortex is considered alive - how do cellular processes continue when the cell wall is stiff (how do molecules pass through)? The cytoplasm region must still be flexible. It's hard to imagine a soft inside of the cell with a hard cell wall - so hard that a human can't budge even a medium size tree.

It is hard to imagine but, cortex is alive. Just like bone tissue, it can be considered alive and yet it is hard as hell. It is like a castle, strong thick walls yet people can live within it just as well


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Why don't viruses cause wounds?
A simple mental model of a viral infection is that an infected cell emits a lot of virions and eventually dies. The emitted virions have a chance of infecting other cells. Nearby cells are at a higher risk of infection.
Based on this model, if one cell in my nose gets infected, I would expect a large part of my nose to be destroyed, as the infection spreads and destroys more and more cells in the same area.

This does not happen! I survived a number of infections and still have my nose. Why?
I know there are "flesh eating" bacteria. Why isn't this the norm for infections? Does a common cold virus or SARS-CoV-2 not infect a lot of cells within the same area?

Sorry for the childish question. I'd truly like to learn the answer. https://biology.stackexchange.com/questions/93782/what-fraction-of-human-cells-gets-infected-during-a-viral-infection says a virus may infect around 0.3% of the cells in the human body. That could still be a visible piece out of my nose!

If you’ve ever had or seen a cold sore, that’s a viral wound. There are others, but not a great deal, and the reason is explained below.

Cells which are infected release interferons which, among other things, inhibit protein synthesis in nearby cells. This reduces the susceptibility of nearby cells and is likely one of the reasons behind tissue infection not perfectly matching your model.

How thick do you think your nose is, in cells? How many cells deep would a virus have to "dig", starting from the inside of your nose, until it popped out on the face side of your nose?

Faulty premise.  Viruses certainly can and do cause wounds.  Measles, Ebola, Herpes, Smallpox... the list goes on.  All of them causing horrible lesions, pustules, and nasty suppurating wounds.

A virus does not destroy that many cells before it is exterminated by the immune system or before the host dies.
Perhaps even more crucially, viruses typically target a very specific type of cell — those on the inner mucal surface of the nose in the case of cold or flu, those of the gastrointestinal tract in the case of stomach viruses, CD4 immune cells in the case of HIV, etc.
Update
As an example of how much time it takes for a virus to eat a noticeable wound, one could take the extermination of the immune cells by HIV - although it does not look as a physical wound, it is one, in the sense that enough of the specific tissue is destroyed to cause a life-threatening condition. It takes about a decade(!) - from the initial infection to the immune system failure.
On the other hand, the lethal effect of typical respiratory viruses is typically via obstructions of the respiratory ways due to inflammation or secretions resulting from the immune response, or via creating suitable conditions for a more serious bacterial infection.

Thank you! This makes sense. So the key is that the targeted cells are sort of rare? Even if the virus kills all these cells in my nose, the loss is invisible? I have no idea what my nose is made up of. But there are parts that I think are largely made up of one type of cell. (Muscles, brain.) Do viruses cause macroscopic damage in those tissues?

@DanielDarabos I think the point is that there are cascading secondary effects that cause more damage once a small number of cells are destroyed directly by the virus. Analogy: if you're stabbed, the wound is just a small hole, but you can lose much blood through it.

Another example of a possible local 'wound' is the anosmia (loss of sense of smell) that occurred frequently with early variants of covid.  There's evidence suggestive that entry, infection and death of sustentacular cells (which support the olfactory receptor neurons) could be a major contributor to anosmia and thus a very specialized wound that, while not visible, has a directly notable side effect.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7488171/

@DanBryant A very relevant example, thank you!

"it does not look as a physical wound" *look like

The innate immune system is remarkably good at providing a first line of defense.  Viruses don't just march into your body uncontested.  They basically have to fight for every square centimeter of ground they claim, and even then, it's a race against time before the adaptive immune system pulls facial recognition on them and sends out hit squads which targets them directly.
That means that viruses aren't necessarily able to infect all of the cells in a particular area of tissue.  While viruses have some defenses against immune systems, their very simplicity limits the tricks they can use.  Flesh-eating bacteria, being much larger and more complex, have more tools at their disposal when it comes to attacking host tissue.
Kurzgesagt has some really good videos on the immune system:

Tiny bombs in your blood - the complement system
How the immune system actually works

The complement system, in particular, is especially interesting, because it's basically a free-floating chemical warfare system which passively protects virtually every part of your body 24/7.  No signalling molecules or specialized immune cells are necessary for it to start interfering with foreign invaders.

@theonlygusti: Change to square micrometre then.

"Flesh-eating bacteria, being much larger and more complex, have more tools at their disposal when it comes to attacking host tissue." One of which being producing toxins (I suppose a virus theoretically could have genes that cause your cells to produce toxins, but they can't produce anything directly).

Smallpox, now eradicated, caused severe lesions. In those who survived: the lesions often turned into scars.

Welcome to Biology.SE. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then [edit] or delete  your answer accordingly. In particular, note that answers should directly address the original question and are much more likely to receive a favorable response if they include supporting references (primary literature is best). A critique should be posted as a comment below the post, not as an answer.

The other answers cover our immune system and the likelihood of viruses surviving it.
Regarding your missing nose:
Do you know how big skin cells are?
Do you know how many need to vanish to leave a visible defect?

As a visual aid, have a look at Genetics Education Site of University of Utah.

A typical skin cell is about $30$μm² - that is really really really small.
Some math:
Using these numbers we can estimate how many cells need to die for a 1mm² defect:

$1$ mm² holds $1.000.000$ μm²

That fits about $33333$ skin cells.
To remove your nose though we need volume - so:

$1$ mm³ holds $1.000.000.000$ μm³

Assuming$^\bigstar$ square-ish skin cells, each cell is about $\sqrt[2]{30}^3 = 165$ μm³ "big".
A $1$ mm³ "hole" has $1.000.000.000$ μm³, that are about $6.06 * 10^6$ square-ish skin cells for a defect that I regularly make while shaving.
And all those damages are constantly under repair by your body.
Summarize:
The danger of you losing your nose from a viral infection is negligible. They tend to spread out and not stay localized, are constantly battled by your immune system and efforts of your body to repair/remove damaged cells.

$^\bigstar$ not squarish - but for simplicity's sake we'll go with that

I'm not sure this really addresses the thrust of the question. I interpret it as; "a virus that initially infects the nose can do enough damage to kill you. How can that much damage occur without the initial site of the infection being totally destroyed." (The answer really being that viruses don't fully conquer one area before moving on but cause small amounts of damage all over the place)

Those huge numbers have no meaning for exponentially multiplying things like viruses...

(1mm)²/(30μm)² = 1,111 not 33,333 are you assuming that the skin cells are 30μm by 1μm? (I mean, they aren't going to be square either, but they presumably aren't that narrow)

("losing" (not loosing - near "The danger".)

@PatrickArtner I can't edit to make that correction (30um²  area rather than the currently 30um) to your answer as it's only one character


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How do molecules find their places?
In many molecular biology animations, a molecule just flies in and goes straight to the right spot. It's clearly a useful simplification, but I'm interested in learning more of the full story.

I guess at short distances the electric polarizations of the molecules pull them into the right spot. But I have no idea what is "short" here, on the scale of these animations.
This all is not happening in vacuum. There must be a lot of other molecules crowding around. (Water at least.) How does all that not clog up these mechanisms? I imagine an ATP synthase accidentally sucking in a stray RNA strand.
I understand the animations are also slowed down a lot, foiling my intuition. Do the molecules just randomly bump into each other SO MUCH that hundreds of times per second an ADP randomly flies into the synthase?

Animation of an ATP synthase with ADP molecules flying in:

Source: http://www.mrc-mbu.cam.ac.uk/projects/2245/atp-synthase
Animation of a DNA polymerase with green donuts (DNA primases?) flying in:

Source: https://dnalc.cshl.edu/resources/3d/04-mechanism-of-replication-advanced.html

Apologies for the childish question! I don't know if it's okay to ask such here.

I'm trying to think through the third point. I read that molecules in room temperature water have speeds around 500 m/s. So they can cross a 50 nm distance (roughly the width of these GIFs I think) 10 billion times in a second. The movement of the arriving molecule is much slowed down then.

Another number! The mean free path in air is around 70 nm. In water, 0.2 nm. They indeed are bumping into each other a lot!

I am voting to close this question as a duplicate of the following: Molecular animations of, say, protein synthesis, are simplified, but how exactly?. This is another related question worth consulting.

@David Yes, thanks! I think an answer with more details would be nice, but the question is exactly the same as mine. Sorry I missed it.

You should be aware that the only aspect of such animations that is based on experimental structure determination is the representation of the proteins and associated parts of the nucleic acids. The movement of the proteins is extrapolated from "still" images and the movement of small molecules is completely invented.

Right, thanks! I love Sean Johnson's answer in your second link. It explained everything I wanted to know.

Check  "Fick's law" and "diffusion coefficients"

It depends on the molecule and the type of a chemical reaction. In simple chemical reactions molecules literally randomly collide with the probability proportional to their concentrations, which gives rise to the law of mass action.
However, in a cell, in addition to simple diffusion of the molecules, there are also means of directional transport of molecules from one place to another, such as membrane transport, transport by motor proteins, etc.

I'd add something about concentration gradients to the simple diffusion part.

Thank you! Good point about the law of mass action. When something is burning, I don't go thinking "how do the oxygen molecules find their way precisely into this reaction". I guess as long as the concentration is high enough, random collisions are good enough. Like for ATP? And for rare or unique molecules we have transport molecules.

@DanielDarabos when something is burning a big part is played by convection - the hot air containing the products of burning (CO, CO2) rises, and the fresh air, rich in oxygen, is sucked in. This is not the same as diffusion, which is random motion of molecules. Also, bob1 in their comment above probably meant the osmosis - which is another mechanism of transport governed by concentration difference.

@RogerVadim There's still a lot of diffusion happening at a local scale in that scenario as far as interactions among molecules; the convection portion is best understood as the mechanism for keeping the concentration reasonably high rather than depleting. An important analogy in biology would be the distinction between mass flow, like blood moving in blood vessels, and the diffusion processes by which nutrients/oxygen in blood actually make it into cells.

@BryanKrause I mentioned convection in connection to fire - I am not aware whether similar directed flows exist in a cell. I also agree that diffusion plays a role in fire - in fact, physically they would often be treated together: https://en.wikipedia.org/wiki/Convection%E2%80%93diffusion_equation

@RogerVadim "I also agree that diffusion plays a role in fire" - right, this was my main motivation for commenting. I think your first comment here about convection could have been misinterpreted by someone else (OP in particular) to think that diffusion wasn't as important there. Yes, convection is important in fire, but they were correct to think about the "diffusion part" that matches up molecules for chemical reactions to be effectively the same in combustion/fire and in a cell, and I didn't want them walking away thinking these were fundamentally different.

@BryanKrause I see what you mean, and I agree with this clarification.


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Minimum growing conditions of a given plant
Micro-algae are organisms that can grow in aquatic environments and use light and carbon dioxide (CO2) to create biomass. Researches showed that Micro-algae biomass can be used as bio-fertilizer.
My mission is : to find which plants in the world are best suited to arid climates and to arid soil that was treated using the Micro-algae biomass.
This is my approach on how to accomplish my mission:
I' m into collecting chemical characteristics data of the soil , chemical characteristics data of the micro-algae biomass and other environmental factors like the temperature, rainfall and humidity of this environment. I want to use this data to determine whether a given plant can survive (adapt) in this environment. So I want to compare this environment (arid + Micro-algae biomass applied) characteristics (N, P, K, Temps, humidity....) to the minimum growing conditions of the given plant .
My problem is : How to determine that minimum growing conditions of a given plant in terms of the needed nutrients (N, P, K) , Temperature, water etc...?
I'm open to any biology/math resources and any other inspirations or approaches.

Depends very much on the plant you are interested in. Better studied ones such as crop plants or things like Arabidopsis will be well characterized; others not so much. Don;t discount things like formation of mycorrhyzal networks.

OK, Currently, I'm targeting plants that are food for humans/animals. Is there any data source of plants that are well characterized (like potato, Onion...). BTW I'm not a biologist I'm a Data Scientist.@bob1

We see this sort of thing quite a lot. To actually answer this question you will need to learn a lot of biology.  Is there a database: probably not (AFAIK), you would have to dig the literature for yourself, and you will find it mostly comes in the form of "plant variety (not species, individual variety within species) grown under abnormal X, but "normal" conditions Y,Z,A,B,C... etc". You might find ranges for some variables in reviews or horticulture textbooks/manuals/gardening guides. Seed packets often have climate ranges for sowing, but you would need to dig climate conditions.

Ok I got this. I think I will just start reading papers and books instead of wasting my time looking for a database. thank you so much @bob1


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How good is the vision of diurnal birds of prey really?
Diurnal raptors (especially eagles and hawks) are commonly thought to have incredible visual acuity, up to 5 or 8 times higher than a typical human. However, I haven't been able to find any scientific evidence of such measurements, beyond popular science websites and unsourced Wikipedia articles. The actual scientific estimates I've seen (such as this, see the results referenced in part 9) indicate that their vision is not really overwhelmingly better than our own, with even exceptionally large raptors like the wedge-tailed eagle only having twice the visual acuity of an average human, and many small sized raptors like falcons having actually substantially poorer vision. I understand that eye size is important (even with their proportionately large eyes they're still not larger than ours, and that places a maximum limit on spatial resolution)
They also have lower achromatic contrast sensitivity than a human (although their ability to distinguish chromatic contrast is far higher).
So are there any actual bird species with 5 times better vision than a human or is it just a pop culture/folklore myth?

Helpful paper https://www.sciencedirect.com/science/article/pii/S1084952119301004. part of the problem is "acuity" is not a perfect term, some eagles can see things from 5 times the DISTANCE humans can.


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Why does the body lose enzymes over time?
I recently started my GCSE Biology course where I spend the next two years learning and preparing for my GCSE. One of the questions I have is that I was told that enzymes are recycled every time they are used. So why do people sometimes refer to developing an enzyme deficiency?

There are conditions (genetic) such as enzyme deficiencies, but the chances of you meeting someone with them in your lifetime (unless you specialize in this medical field) are infinitesimal. I'd take what people have to say about themselves with a pinch of salt - as claiming bizarre medical conditions comes into fashion frequently, particularly since the advent of Wikipedia. That being said, you never know.

@ARogueAnt. Glucose-6-phosphate dehydrogenase deficiency is an obvious exception. (Such individuals (over 400 million worldwide) are sensitive to fava beans, for example)

Good point, now I think more about it, digestive enzymes relating to dairy come to mind too, so developmental pathway differences fit also. @user338907

Proteins are fairly fragile molecular machines. They are subjected to environmental and intentional degradation all the time. There is quite a bit of variability across different protein types in how long they last, but none are permanent. Chen et al 2016 write:

For example, RALB is a GTPase, and is involved in a variety of cellular processes including gene expression, cell migration and proliferation, and membrane trafficking. The half-life was measured to be 9.4 hours in this work. IGFBP1 is insulin-like growth factor-binding protein 1, which is a well-known secreted protein. It has a very short half-life of 0.3 hours inside the cell because it is secreted after synthesis. The distribution of all protein half-lives is shown in Fig. 4b. The bin at 9 hours (half-lives between 8 and 10 h) contains the greatest number of proteins. The majority of the proteins quantified have half-lives within the range of 4–14 hours. About 6% of all quantified proteins (49) have half-lives <4 hours, while 51 proteins have long half-lives (>14 hours); the median half-life is 8.7 hours.

When someone talks about enyzmes being "recycled" in a reaction, they're contrasting between enzymes that participate in a reaction but yet are not consumed in that reaction, and other chemical species that do in fact become consumed in the reaction. That doesn't mean that an enzyme is indestructable, just that it isn't used up in the reaction itself.
Similarly, a wine glass is not used up in the process of drinking wine. It's recycled every time it's used. And yet, in the course of being used or even just sitting on the shelf, a wine glass is subject to degradation in the environment at some rate. If you never ever purchase another wine glass, or at least don't purchase them as often as they are broken, you're likely to over time develop a deficiency.
For normally functioning proteins in normally functioning cells, the proteins that are degraded are constantly being rebuilt from scratch. To have a deficiency would require something in the process to go wrong: either degradation is too fast, or something along the chain from DNA -> RNA -> translated protein -> post-transcriptional modification and transport is slowed down or incorrect.

Chen, W., Smeekens, J. M., & Wu, R. (2016). Systematic study of the dynamics and half-lives of newly synthesized proteins in human cells. Chemical science, 7(2), 1393-1400.


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Identifying substance in body fluid (serum, urine)
I have a large number of serum and 24 hour urine samples from a collection of individuals on many consecutive days. Some of the samples contain a 'large' amount of a substance that has a brown color. The concentration is large in the sense that there is a visible discolouration in those samples. I want to identify the most abundant molecules that are causing the discolouration with some degree of accuracy.
Is it possible to analyse by chemistry methods?

I’m voting to close this question because it doesn't appear to be about Biology as defined in the [help]. This seems like it would be a much better fit in either [Chemistry.SE] or possibly [MedicalSciences.SE]. However, please do not crosspost, instead either request migration or delete from this site before reposting.

Of course it is!

Dipstick urinalysis?

source
The urine dipstick has a bunch of squares, each with a chemical analysis ready to go.  The dip will semiquantitatively show you what is in the urine.  My bet would be hemoglobin but various urine dipsticks will have various substances on there.  A dipstick will detect hemoglobin which will come out of any blood cells once they lyse on sitting in storage for a while.  Free hemoglobin can be in fresh urine too if a person is hemolyzing.  Another brown thing could be bilirubin.  All detectable with chemistry.
A serum chemistry lab will quantify many different things in serum - again bilirubin would be my bet as a common component of serum.  You can look for almost anything and a clinical lab can run a chemistry test to determine presence or quantity of that thing.
Chemistry tests could miss nonchemical microscopic brown things.  Bacteria or mold could contaminate your specimens, or there might still be red blood cells present.  You could look for these things under a microscope.


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Evolutionary advantage of the nutrient played by the chicken
What is the evolutionary advantage of the chicken throwing out so much nutrient ovulating all the time?
Is there a clear advantage to this? Chickens ovulate all the time for the same reason human females do, when the egg is not fertilized it is discarded, in the case of the hen it lays an egg, in the human case menstruation occurs. This is due to the rhythm of reproduction of each species, if the egg is fertilized, it is an advantage that it can fertilize all the time.

First, most chickens will not naturally lay an egg every day. (I raised hundreds - yes, hundreds - of chickens.) It varies, with some breeds (selected over many decades, some hundreds of years) being "heavy layers" and others absolutely not. Also, artificial light and heat is needed to produce eggs year round. If there are roosters around, trust me, almost all (if not all) of the eggs will be fertilized. I used to hatch out my own chicks from fresh eggs collected in no particular manner. I never had a dud. Today's commercial and farm chickens are not the "originals".

@anongoodnurse in the end is it useful to lay a lot of eggs by artificial selection, in short?

Be careful you aren't doing something akin to asking what the evolutionary advantage of a seedless orange or grocery store banana is.

It is useful to humans selling and buying them for chickens to be forced to lay eggs every day, yes. Does that take a toll on chickens' lives? Yes, a great toll. My chickens did not lay eggs every day, and were not killed when production decreased. In return for having been selectively bred for egg laying, and doing so for me, I gave them a good life. I did not force them to lay eggs in any way.

@DKNguyen but seedless fruit only exists transgenic, no?

@Behemooth Not transgenic. Seedless fruits are a naturally occurring mutation that would have otherwise died out but was found and artificially propagated. Think about it...what organism would you even get a seedless gene from to insert it into something to begin with?


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Where can I obtain Sputnik virophage samples?
I'm working on a project where I'm trying to use virophages as viral vectors in introducing CRISPR-Cas proteins into other viruses. I was wondering where I might be able to find replication-defective Sputnik virophages or other virophages for this kind of experiment?


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A study has found that cell phones cause infertility, is this something to worry about or is the study flawed?
Is this a worrying study, or is it flawed?
A study has found that cell phones are detrimental to male sperm quality (Lower sperm motility and sperm concentration). It’s original goal was to determine if image content has a effect on sperm quality, but accidentally discovered that men who said they kept their phone in their pocket had worse sperm quality than those who didn’t have a phone in their pocket. As far as I can tell, from my limited knowledge, the study isn’t very flawed. What I do know is that they used 52 men, which doesn’t seem like a lot.
Another possible flaw is in regard to how they took sperm samples. Sperm parameters can vary amongst healthy individuals, the WHO recommends taking at least 2 samples to determine fertility. This study took one sample from all 52 men, then asked them if they wanted to participate the second time around and only 25 men agreed. So, they did take more than one sample but only for 25 men. I’m not sure, but this doesn’t seem like very good methodology as only 25 of the samples are representative.
Another issue is that the study had a variable that it changed from person to person. As stated, it’s original goal was to find out if image content affected sperm quality, and they concluded that it can. They gave different images to each mam, meaning that some of the images would have had a detrimental affect to the sperm quality. So, they could have gave a healthy cell phone user a type of image that causes poor sperm quality. However, it would be coincidental that cell phone use was still correlated with poor sperm, even if the study randomly gave out out different images to different people that could cause poor sperm in the analysis the ones with poor sperm.
I was wondering if certain lifestyle factors that tend to be associated with phone use where causing the infertility, not the phones themselves, but the study had a very extensive questionnaire and adjusted for many different factors from bathing habits to diet, so I don’t think that the study can be flawed in this are. What do you guys think? Is this something that we should be worried about and change our habits over, or is it scientifically limited and no cause for alarm until bigger and better studies conform their findings?

The effect was 49.3% plus-or-minus 8.3%. Not a worry. I couldn’t get the data on how many carried their phones in pocket.

In addition to the dubious quality of the study, why would one necessarily worry about infertility?  After all, quite a bit of effort has been devoted to the development of male contraceptives, so far unsuccessfully AFAIK.  If a simple and fairly inexpensive electronic device could do the job, and also let you make phone calls & check your email, we should be celebrating, not worrying :-)

@PolypipeWrangler what do you mean by ‘The effect was 49.3% plus-or-minus 8.3%’?

@jamesqf firstly, few men using contraceptives choose pernanent snd irreversible contraception; secondly, here they don't even make a choice - they might be rendered infertile without wishing it.

@Vadim: Does the study claim that the supposed infertility is irreversable, or just a temporary effect?  As for the choice, any and every action will have unforeseen consequences.

The study is basically worthless.
First, the study was not constructed to test this hypothesis, so it's just something interesting that may point to future studies. It does not provide sufficient evidence.
But the biggest problem is that the study was of 52 individuals with only one or two samples, which makes it statistically useless.
Any uncontrolled variable could account for all the difference detected. If one person had low sperm count because they wore tight underwear it would completely account for the difference.
This would barely qualify as an exploratory study, much less anything conclusive. This study would need to be reconstructed with a minimum of thousands of people, or control the participants' behavior (preferably both), to produce useful conclusions.
Any study with a really small N that deals with human behavior is basically worthless as far as any certainty goes.
The questionnaire is not any better — cellphone position is just binary: 1 belt and/or pocket, 2 anything else. Since most of the people are going to fall in the first category, there are very few degrees of freedom to work with. They just ran all the numbers hoping to get something. This is barn door statistics at its worst.

Thank you! The study did have a relatively good questionnaire which account for thing like diet, tight underwear, etc. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1617155/bin/rsbl20050324s01.pdf) But I take your point over the small sample size. Do you think that the fact that the study was done in 2004, a time when phone where very different to what they are today, makes it hard to apply their results to the modern day world?

the sample size makes the outcome useless any variation could be entirely do to outside events. the issue with questionnaires is people get answers wrong. "my underwear's not tight this is how you wear them" large number help wash out these errors. also check out the survey, the options for phone are 1 "in pocket or on belt" 2"everything else" which is bad construction. all those questions on the survey actually make it worse, with the tiny N it becomes impossible to check for confounding between variables. there literally is not enough degrees of freedom to account for all variables.

thank you so much! So you think that nothing should be concluded because of this study? Or, at least nobody should avoid using a phone because of it?

Yes nothing can be taken from this study, its not even worth giving consideration too.

Thank you so much! This has been really worrying me for a year now and I’ve been avoiding using a phone around people out of fear it would make them infertility. May I ask how you know so much about this area of science?

Its just basic statistics and experimental design. which is why I argue the basics should be taught in primary school. recognizing bad statistics in not too hard but it is not taught. I minored in statistics but you really don't need to know any the the math involved to stop such problems.

@John — Your post came up in the edit queue. I improved on the suggested edits by adding a link to what I infer you mean by "barn door statistics", but I'm letting you know in case I guessed wrong!

@tyersome that is it exactly.  thank you;.

You're welcome! An added bonus is this means I've leaned a new term today.


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How to find the origin of each Single Nucleotide Variants (SNV) in child when having variant call data for both parents?
I am working with a trio (Mom, Dad, Child). I have variant call data for all three. Now I want to know each SNV in the child comes from which parent?
Is there any tool that could help me to achieve this goal?
Many thanks,
Vahid.

I think this is more suited to the Bioinformatics beta. If the post is migrated there, I can help you, as long as you give more information on the kind of data you are working with. Note, there is a plugin called parental-origin in bcftools which does what you need.

If a SNP is present in a child it is also present in at least one of the parents (except for de novo mutations which are fairly rare). So just check which parent has which polymorphism. For a question like that you would write a script yourself to check that.


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What causes eye strain when viewing any display?
Few everyday experiences:

Staring at the physical paper (or any other sight in nature) doesn't cause eye strain.
Staring at the LCD screen causes eye strain.

Some of the differences in properties I have isolated so far are:

Refresh rate, that how often picture updates itself. For LCD like display, it is finite, but for the physical paper (viewing up, down or turning page) it is instantaneous (infinity),

Most common LCD emits backlight to project image, whereas physical paper reflects light.

Other effects like glare, blue light (harmful light which disturbs sleep cycle)  which is absent in physical paper but present in most of the LCDs.

(3.1) The physical paper doesn't distort contrast or image quality whereas LCD can sometimes. Although I am not sure how giving an inaccurate description (which is a different problem) can cause eye strain.
So I want to ask what makes up a favourable viewing experience from a biologist perspective.

Biologically you need to use soft light if your eyes are forced into a fixed distance on small details, then at least there shouldnt be bright lights all around the small details. 1/Try alt-control-print buttons if you have windows. It inverts the colors white on black. 2/install "gamma panel" you can fix hotkeys to different brightness levels, i.e. I have ctrl-f1 to f5 instantly change brightness effortlessly. 3/dark reader for chrome. fixed eyes. on android say "accessibility"and find the vision/invert colors option... and use n offline reader which reformats text size and colors.

Any task that implies an intense use of the eyes may cause eye strain. The difference between reading paper and staring at a screen may vary from the distance, pauses made when turning the page, etc...
As stated in this link, it depends on the individual. So a favorable viewing experience is any that does not require an intense effort given the particularities of the subject's vision.
"Some people, while concentrating on a visually intense task such as reading fine print, using the computer for hours at a time, or trying to see in the dark, unconsciously clench the muscles of their eyelids, face, temples, and jaws and develop discomfort or pain from overuse of those muscles. This may lead to a vicious cycle of tensing those muscles further and causing more distress. Other people attempting to do similar visual tasks may have no symptoms at all."
https://www.medicinenet.com/eye_strain/article.htm#what_causes_eye_strain


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How do mothers handle acid from embryo bone mineralization?
This is a relatively trivial question, but, I have not seen it discussed much. It could be one factor in the "acidosis of pregnancy" (JAMA, 1929). Are the compensatory mechanisms measurable, by dietary phosphate requirements increase by 3 mmol (40% more than adult average of 7.4 mmol) or something similar?
A human fetus  acquires 30 gram of calcium during pregnancy (Kovacs, 2014). The molecular weight of calcium is 40 gram per mole, 30 gram is 30/40 = 0.75 moles. Bone mineralization releases hydrogen ions since bone mineral requires hydroxide ions (Bonucci, 1992). Calcium and hydroxide ions have a 5:1 ratio in bone mineral, bone mineralization during embryogenesis releases 0.75/5 = 0.15 moles of hydrogen ions, 150 mmol.
80% of this H+ is generated during the third trimester of gestation (Kovacs, 2014), with up to 1.5 mmol per day (300 mg calcium/day, see Kovacs, 2014) between weeks 35 and 38. When 1.5 mmol H+ is distrubuted on an average 70 kg body, with 60% water, 70 kg * 60% = 42 kg = 42 L of water, the molarity is 1.5 mmol/42 L = 0.035 mmol/L. This is equal to -log10(0.035 mmol) = pH 4.45.
References
THE ACIDOSIS OF PREGNANCY. (1929). Journal of the American Medical Association, 92(25), 2104. https://doi.org/10.1001/jama.1929.02700510034014
Kovacs, C. S. (2014). Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones. Physiological Reviews, 94(4), 1143–1218. https://doi.org/10.1152/physrev.00014.2014
Bonucci, E. (1992). V. Regulation of hydroxyapatite formation. In Calcification in Biological Systems (p. 134). Boca Raton: CRC Press.

1.5 mmol/d is nothing. By some estimates, a typical adult produces non-volatile acid at 70 mmol/d even in the non-pregnant state. (This includes H+ as a by-product of metabolism, from the diet, and due to intestinal losses of bicarbonate.) How this 70 mmol/d is handled makes for interesting reading. I believe the same processes also handle the excess H+ produced by the foetus in pregnancy.


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Can I reuse agar in Petri dishes?
Can I simply re-melt agar in a contaminated Petri dish to use it again? I've tried searching for the answer on the Internet, but I was only able to find information about reusing Petri dishes themselves, not the agar in them.

reuse for what?, plant food, sure, for an experiment, no, spores are things.

@John Microwaving does not destroy the spores?

No, not just heating it enough to melt, many spores need prolonged heating to be destroyed  and some spores can survive anything short of incineration. Your not just talking about human dangerous spores, a plate can be contaminated by all kinds of spores.

Depends on what the dish is made of - plastic ones might well melt.

Is it a broth agar or other with some nutrients in it? If so, once used some (a small fraction or more depending on how heavy the growth was) will have been used up, and there will be an accumulation of metabolic byproducts, so newly plated growth may be affected. You also run the risk of not eliminating all microbial contaminants. If you're a hobbiest, it might not matter to you (eventually the agar will be useless), but if you're serious, the answer is to stick to accepted protocols.


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Does this explanation hold good even in case of Mitotracker red?
When the fluorescence intensity is higher when the depolarization is high?
The more damage to the mitochondria, the more mitochondrial dysfunction and therefore more fluorescence intensity. So, in irradiated cells(), 2, 5, 20Gy); the Mitotracker Fluorescence intensity will be lowest in 0GY and highest in 10 gy.

No, the Mitotracker probes accumulate in active mitochondria, not in ones that are dysfunctional, as mentioned in the product page from Cell Signalling Technologies (emphasis mine):

...with MitoTracker® probes, which passively diffuse across the plasma membrane and accumulate in active mitochondria.


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Determining the Length of DNA in a Human Spermatozoon
Hello everyone,
I’m currently trying to solve a problem related to DNA length in human spermatozoa and could use some guidance.
The problem states: “The DNA of one human spermatozoon contains 10^23 pairs of nitrogenous bases. Determine the length of the DNA molecule in a human sperm.”
I know that the distance between two base pairs in a DNA molecule is approximately 0.34 nm. So, I’m thinking that I need to multiply the number of base pairs by this distance to get the length of the DNA molecule.
However, I’m not entirely sure if this is correct or if there are other factors I need to consider. Also, I understand that this calculation will give an approximate value and the actual length can vary depending on the specific sequence of the DNA molecule.
Could anyone confirm if my approach is correct or provide guidance on how to accurately calculate this length? Any help would be greatly appreciated!
Thank you in advance.

Hi Wino, welcome! Is the question about bp length or actual length? If this is about bp length then I think the answer is in your question. Maybe there is some additional context to the problem?

This site is not a service for people to check their homework before submitting it. Please desist.

10^23 is an absurdly large number. Should be 10^9 ish. Approach seems correct. There is a book Cell Biology by the Numbers which you can use to verify your answer.


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Does having to urinate imply that you are becoming dehydrated?
This question came up after I read another question that coffee does not dehydrate you, but instead acts as a mild diuretic.
Does having to pee imply dehydration?
Allow me to elaborate: When you have to pee, that liquid is already in your bladder, right? If so, it is not in use by cells. However, since that water must have been previously absorbed in the body in order to be filtered through the renal system, having to pee indicates that you are less hydrated than you once were.
So in the case of coffee, while it doesn't directly dehydrate you, doesn't it indirectly dehydrate you by causing you to pee?

Hm, aren't you forgetting that you are ADDING water to your body by drinking coffee?

Also, there are two common ways of describing "wanting to pee". There is "frequency" (feeling like you're going a lot) and "urgency" (if I don't go in the next 10 seconds my bladder is going to explode).

There are two parts to answer this question. "How does my body know when to pee? Do diuretics affect that, or my hydration?"

Does wanting to pee imply dehydration?

In summary: Not necessarily. Your body might have plenty of water, but the bladder is full. Alternatively your body might be dehydrated, but the caffeine and normal body functions have filled the bladder and you'll need to pee.
Caffeine as a diuretic.
Caffeine belongs to the Xanthines, and inhibits reabsorption of Na+ by cells, and increases flow rate of filtered fluid through the kidneys. This reduces water content in your body. In other words diuretics do dehydrate you, specifically caffeine will. Coffee and tea (very low doses of caffeine) are mild diuretics.
Bumetanide, Furosemide, and Torsemide are examples of stronger diuretics, and hydration should be monitored closely.
On the other hand, the colour of your urine may indicate your hydration.
The below image is a crop of this Cleveland Clinic infographic.

How does my body know when to pee?
The bladder is hollow and slightly elastic, so as it fills with urine it expands. A healthy bladder can hold up to 2 cups of urine comfortably for several hours. When the bladder approaches its maximum capacity, signals are sent to the brain, letting the body know that it is time to urinate.
But it's critically the kidneys that are controlling the production of urine.
Caffeine increases the production of urine from the kidneys, and fills the bladder quicker. However, the increase in production of urine from a cup of coffee is more than offset by the water in the coffee.