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Can plant fruit and seeds be albino like animals?
There are numerous examples of albino animals, including snakes, birds, fish, mammals---humans too. Apparently this comes from some a genetic defect that results in lack of pigment.
What about plants? Obviously a lack of chloraphyl would be fatal for a plant, so I'm imagining the seed or fruit being white. Does this exist in nature?
Edit: I'm thinking of fruit/seeds that are not normally white.
Note the wiki page I cited has only 2 paragraphs on this:

In plants, albinism is characterised by partial or complete loss of chlorophyll pigments and incomplete differentiation of chloroplast membranes. Albinism in plants interferes with photosynthesis, which can reduce survivability.[4] Some plant variations may have white flowers or other parts. However, these plants are not totally devoid of chlorophyll. Terms associated with this phenomenon are "hypochromia" and "albiflora".[5]

That last part seems what I'm interested in, but the cite is a dead link.
Later in the article:

The primary function of pigments in plants is photosynthesis, which uses the green pigment chlorophyll along with several red and yellow pigments including porphyrins, carotenoids, anthocyanins and betalains.

No cite there and not much info anyway.
So are white seeds or fruit found in nature?
If you're curious, I originally thought of this as an alternative way of getting white chocolate from an albino cocoa bean, and maybe even a white coffee bean too.

Coffee beans are green before they are roasted; the brown color comes from the Maillard reaction (and possibly some caramelization), same thing that makes bread brown on the crust, and chocolate as well. Coffee or chocolate without the color wouldn't taste anything like normal. And white chocolate isn't really chocolate, it's a candy made with only the "butter" from cocoa beans which is really just a vegetable oil.

@BryanKrause Right that is why I wanted a "real" white chocolate, tho ofc who knows what it would taste like. I didn't know about the green coffee beans tho. Interesting.

White seeds: rice? White fruit: banana (not the peel of course)?

Great place for me to plug the super interesting story about  albino redwoods

@WYSIWYG Was thinking more like seeds/fruit that are not normally white but have suffered an albino gene.

@DrZ214 What about the classic finding of transposition in maize kernels by Barbara McClintock? That is, of course, within the same organism. There are variegated leaves too. Some vegetables also show variegation. There are white eggplant varieties. Do any of these examples fit your query?

@WYSIWYG I supposed it's a question of what exactly is considered an albino gene as opposed to a "normal" gene responsible for white or yellowish-white that we would not consider defective. Corn, maybe, but yellow and white could be kinda a gray area. I have never heard of white eggplant so I think yes there, but OTOH squash is yellow and eggplant and squash are very similar. Interesting, tho, that all those examples are vegetables and not fruit.

@DrZ214 Eggplant is a fruit.

@WYSIWYG Is it really? Yikes, it is. And it's a berry too? I'm sorry but what a terrible thing to classify as a berry IMO. It's a good thing we have genetics to use instead of tastes.

Do flowers count? There are some species where part of the population is white, e.g. Frittellaria meleagris

@RHA As far as I can tell, yes those count.

Don't know whether it counts as albinism, but there are quite a few white fruits out there.  Off the top of my head, there are white pumpkins, white corn, white peaches, white carrots,..

When thinking of albinism in fruits, the only thing I could think of is strawberries. Yes, there can be albinism in strawberries! They are nearly always assocoated with excess nitrogen and are usually tasteless. According to a research by Lieten et al, their mineral composition also differes. Albino strawberries contain higher N:Ca and K:Ca ratio than normal fruits. Another study by Sharma et al shows that albino strawberries show less lipoxygenase activity. Also, Hwang et al and team found that presence of more than normal silicon also causes, among many other things, albinism.

You can get more information here, here, here and here. Obviously, there could be numerous other examples, but albino strawberries is all I could remember.
PS the exact genetic cause and mechanism of albinism in strawberries is not known yet. When searching online, I only found a study by Plante et al which suggests presence of mixoploid cells over a critical number which might have an effect on it.

That's neat! Can they be safely eaten? Do they taste bad? If it's only a nutrient problem that causes it, and not a gene, then there must be some technical definition that I don't know that might exclude them.

Most probably the exact cause is not known and must be genetic. Also, they are mostly tasteless, but not harmful.

Interesting, so it could be a genetic defect that causes them to take up too much wrong nutrients. BTW you should get +1 just for that new link to acadamia. I've never seen a in-html paged document that loads so fast plus word searchable with CTRL+F like normal. Everyone else does pdf.

Albinism is very rare in plants, because most plants can't survive long without photosynthesis. A notable exception is Sequoia sempervirens, an American tree that seems to be able to survive as albino through parasitism. Source

In some plant species with coloured flowers, some specimens are white. A good example is Fritillaria meleagris, for a photo of the white flowers see the Dutch wikipedia page.

Another example of white flowers is Corydalis cava.

However, this is not true albinism, because green parts of the plant are not affected.

Good answer, +1! I've added photos and corrected links, feel free to roll back :)


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Why is the heart not in the middle of the body?
All mammals that I can think of have a high degree of bilateral symmetry (In fact, almost every animal I can think of is like this).
So why is the human heart not exactly in the middle of the body? An effect of this is that one lung is slightly smaller. Are there any evolutionary theories on why this came to be?

You could ask that about all organs of which there are only 1.

@RichardTingle Not exactly all. The brain, esophagus, nose, and even skin itself all maintain pretty good bilateral symmetry. The stomach, liver, spleen, etc. might make good questions but could get closed as too broad if done all at once.

The reason you think your heart is off-centre is that, when you put your hand on your chest and feel your heart beating, you're actually feeling the blood pulsing through your aorta. Your actual heart is hidden behind your breastbone so you can't feel it.

@DrZ214: It could easily be argued that we really have two brains, in much the same way that we have two lungs.   But we only have one liver...

Possible duplicate, https://biology.stackexchange.com/questions/5588/why-is-most-life-symmetrical-externally-but-not-internally?noredirect=1&lq=1

First of all, let me make it clear that the heart is at the vertical centre of the body -- it is not shifted towards left (or right). However, it is slightly tilted towards the left in most cases.

In some cases, it is tilted towards the right, and the condition is called Dextrocardia. For why it is so, lets look at what the heart does. Below is a diagram of double circulation (from here).

As you see, the highest pressure needs to be generated for pumping oxygenated blood into the body. Thus, the left ventricle needs the thickest muscles for this purpose. And due to these extra muscles, the  heart appears extended and seems shifted towards left.
Coming to the evolutionary perspective, it is important to mention that humans are not the only organisms with this feature. Indeed, displacement of the heart towards the left is a conserved feature in all vertebrates (Fishman et al, 1997). See this answer for more information.
Coming to genes, bending of the heart towards one side is actually controlled by the NODAL gene during development. See this diagram (from Jensen et al, 2013):

Tilting occurs in two phases, one during the first four and a half months of intrauterine life and the other, which is actually a 45° rotation to the median plane, later. During the early development of the heart, a process called cardiac looping happens and the straight heart tube develops a bend (see diagram). The NODAL gene, along with the Lefty1 and Lefty2 genes, regulates the speed and direction of cardiomyocyte movement during the development of the heart, leading to this asymmetry. To confirm it, researchers knocked out the spaw/nodal gene from a zebrafish and found randomized development of heart, even symmetric heart, as the result(!) (see Walmsley, 1958 and Rohr et al, 2008).
Now, talking about why this happened in the first place, and why it is so conserved among vertebrates, we need to ask ourselves a basic question: what good would a symmetrical heart be? External symmetry is preferred (probably) because it helps in locomotion; it would be quite difficult to move with your two legs placed away from your center of gravity. But when we talk about internal symmetry, conditions drastically change. We get a major restrictive factor here: space. And limited space always dominates other factors. Seeing that the structure of the heart is necessarily pointed towards one side, it becomes difficult to make it symmetrical. (The only option IMO is to have another pointed end at the right side.) In this case again, what advantage would a symmetrical heart provide? None. And it might even be harmful since having an even bigger heart would mean making both lungs smaller. Thus, a symmetrical heart would only prove to be a liability rather than an asset. See this question for more information.

This is a pretty amazing answer, even giving detail of heart development in the womb. Thanks! If you ever come across an evolutionary theory explaining this, please come back and link to it.

@another'Homosapien', how on earth do you know so much about this?

Our bipedal stance would also come into play. the torso is in a vertical position with respect to gravity, as opposed to the regular horizontal, so the pumping would be more difficult against other vertebrates of our size.
How is the poisitioning in the great apes?

After almost 10 years in academic biology, I stumble across this question and learn that the heart is in the middle of the torso. Thanks, my mind is blown (and +1 of course).

@another'Homosapien' considering that all the reasons you mentioned in your answer could be satisfied without breaking bilateral symmetry  if the heart was oriented dorsoventrally  is there any evolutionary reason why the heart is oriented laterally rather than dorso-ventrally ? i understand that symmetry _by itself _ is not a feature that evolution tries to achieve but is there a reason for this anyway? excellent answer by the way......

I guess it is elusive in a way... Just thought there should be a reason since the majority if not all species with a structure similar to humans have the same orientation. Although now that I think of it the size does seem to be a plausible reason. And sure thing.. I'll hold my vote until tomorrow :)

Very good answer. Here is a broader view to show the location almost at the center : from a cnbc article   (feel free to add this into your answer ^^)

"it is not shifted towards left (or right). However, it is slightly tilted towards the left in most cases" - Clearly, the center of mass of the heart is off-center because of that tilt. Sufficiently such that the left lung is smaller than the right, and has a different pattern of vascularization. I do still think it is more centered than most people conceptualize, though, so I agree with the overall point, and your description of the development is excellent, thank you.

I just joined this site to upvote this answer. Amazing answer! Thanks for this information. I wish I could give 1k upvotes to this answer.

@bryankrause yeah, certainly it is not in exact middle if you see it from average mass, but also certainly it is not off-center if you see it anatomically...there can certainly be confusion about this ;)

To confirm it, researchers knocked out this gene from a zebrafish and found a symmetric heart as the result(!) (see Walmsley, 1958). You've cited the wrong article...

And due to these extra muscles, the heart becomes a little tilted towards the left. Do you have some kind of reference for this statement? The asymmetric nature of the heart seems more a happenstance of development that doesn't require, nor even warrant, such an explanation.

What is the article? 1958 is well before any knowledge of developmental genes. 2) My point is that even if the ventricles were the same size, the heart would still be on the left side.

@canadianer 1. I'll look for it then ;) 2. Well...the bigger size of LV definitely does contribute to the appearance. I mean, just crop the bottom right part of a heart's image and paste it at bottom left...would definitely look different. Now, lets remove these comments now, for obvious reasons :P

Now this is an answer that goes to the heart of the matter. Good job!

1- Bilateral symmetry means two mirror image halves following sagittal section only along a central axis.In animal kingdom there are examples of no symmetry (amoeba) , radial symmetry (jelly fish) , biradial (comb jelly and bilateral (human - though not exhibiting perfect bilateral symmetry because of heart, gall bladder and liver)
     Heart is not symmetrical on account of its functions -the left ventricle is thicker compared to the right).The smaller Left lung could be the result of a varying functional load associated with oxygenation of the blood.

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Two 20 million yr old fossils of Hummingbirds found "The amazing thing about the fossil is that it's essentially a modern hummingbird
does this only mean that the Hummingbird is perfect in creation and needs no change to survive?
http://news.bbc.co.uk/2/hi/science/nature/3691169.stm

Please add references/links to your claim.

The report does not say "exactly identical". The BBC news feature say the fossils "show many striking resemblances to modern hummingbird groups". The primary article (http://www.sciencemag.org/content/304/5672/861.full) says that the extinct species "is of essentially modern appearance and exhibits morphological specializations toward nectarivory and hovering flight". Your premise is wrong.

Nothing puts a biologist off as quickly as a phrase like "perfect in creation". Biology is a mess; see this xkcd to see what I'm talking about.

Hummingbirds were not created, they evolved.
Ancestors of a modern species need not be that morphologically different from their progeny, even over a time span of millions of years. And organism will fill a niche based on its fitness to survive in the niche.
If there are strong selective pressures in the environment to maintain the traits that we see today, even over a 20 million year time horizon, those traits will be preserved. That means that any variation that may have occurred, that does not confer a survival or a reproductive advantage, will be lost to the traits that are selected for.
You then also have the idea of coevolution. If a particular flower that produces nectar that the hummingbirds relied on as their only source of food, could only be pollenated by the hummingbirds, then they would also rely on the hummingbirds. The success of each organism relied upon the success of the other. So the adaptation that made the hummingbird successful at feeding from that plant also made the plant a better breeder, so as both succeeded, but both relied on specific traits of the other, then they both put pressure on each other to stay relatively the same.
Add to that, if the niche was such that the hummingbirds didn't have a significant threat from predators and the plant didn't have parasites or other invasive species that would kill it off, and no other plants in that niche evolved as a food source for the hummingbirds, then there really is very little selective pressure for change, and the traits of both can be maintained for long periods of time.

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Could a prolonged amount of Antibiotics severely affect the digestion Gut Microbiota?
Could taking antibiotics for a prolonged amount of time severely harm or even worse kill off a large proportion of Gut Microbiota responsible entirely for  digestion, Resulting in lifelong digestion problems similar to Crohn's Disease?

I’m voting to close this question because it is more suitable for SE Medical Sciences, which did not exist when it was originally posted.


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How can I perform virus neutralization assay for influenza?
How can I perform a Virus Microneutralization assay for influenza virus using serum from mice vaccinated with this virus?

There are a number of different protocols, but the canonical one is published at the WHO Influenza site:
SEROLOGICAL DIAGNOSIS OF INFLUENZA BY MICRONEUTRALIZATION ASSAY
It gives a detailed, step by step protocol.


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Can anyone tell me what type of snake this is?
I found this snake in my garden and I'm wondering what type of snake it is! It was around 1 metre long and I'm in Lincolnshire UK.

It was around 1 metre long and I'm in Lincolnshire UK

With all due respect, it's fairly common knowledge that there are (essentially) only 4 native snakes in the UK: the adder, grass snake, smooth snake and barred grass snake. If you see a snake in the UK, chances are it's one of them.

I believe this is a Barred Grass Snake, Natrix helvetica. There are only a few snakes naturally found in the UK, and the Grass Snake matches the size, color, and pattern (bars on the sides but not on the back). The "N. helvetica" designation is relatively new, 2017, following genetic testing that showed that the previous name of Natrix natrix was not correct. "The newly distinguished snake is grey, not olive green like the N. natrix and does not have the same bright yellow collar."

Youtube video
Stock photo from Alarmy
Publication describing geographical distribution: Phylogeography and taxonomy of the barred grass snake (Natrix helvetica), with a discussion of the subspecies category in zoology. Figure 1 (below) includes a photo

Smooth Snake is another possibility but seems much less likely to me.

Smooth snakes are slender and normally grow to around 55 cm (2 ft). They are grey or grey-brown with darker markings along their back and usually a 'butterfly' shape on the top of their head. They are very rare in the UK but can be found in heathland habitats in Surrey. It would be very unusual to find a smooth snake in your garden. They are very secretive and would normally be found underneath objects.

--Which snake is it?
 (My emphasis)

Smooth Snake.
1 Metre long is a bit large for this species, but it is in that range and it is where you live.

Both sexes grow to an average length of about 60 cm (24 in) to 75 cm (30 in). Two specimens measuring 83 cm (33 in) have been recorded in Sweden, as well as one in Russia that was 92 cm (36 in).
[...]

 Smooth Snake - Wikipedia

Here is another picture of the snake, which seems almost identical to yours.

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Serotonin activity with short 5-HTT promotor region and depression
So after reading a few studies (1,2) it seems that a shorter promotor region for the serotonin transport protein may be associated with increased likelihood of developing depression after stressful life events.
I'm still an undergrad but this would seem like it would lead to less transcription of the protein leading to more serotonin at the synapse. My understanding is that this should then lead to some sort protection against mood disorders not the increased likelihood of them like the studies suggest. Is someone able to explain what I'm missing here?
Thanks,
Zane


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Which spider(?) is this hanging out on my seaside daisy?
The title says it all... location: Switzerland

These things are very shy (of humans, anyway), but great ambush hunters.  I watched one wait patiently on one side while a hoverfly explored the (comparatively) vast surface on the other side of a gaillardia, until the hoverfly chanced within range of the crab spider, whereupon it pounced with great rapidity.

Misumena vatia. (Crab spider, female specimen.)

OZGUR KEREM BULUR / SCIENCE PHOTO LIBRARY 2022, fair usage.
Size: Females can reach 1 cm at maturity, males half that size.
Comprising more than 2000 species, crab spiders can be found all over the world, with the Mitsumena Vatia being confined exclusively to Europe and North America.
A kind of active camouflage allows them to change colour with each moult in response to their surroundings. Colours and intensity of marking varies, the body being yellow or white, the markings pale through intense red and green.
Females are mostly static and wait to catch prey on flowers, trailing a silken line which the males follow to find them.


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Is there any way to cultivate viruses without cells?
I know what viruses are. They replicate only inside the living cells, and so on, and so on.
I just interesting maybe there is some progress in this field. I don't know exactly, but I suppose before invention of the nutrient agar microorganisms were cultivated on substrates like eggs, potatoes, meat etc. Perhaps there is the same story for viruses.

No. A virus is a small infectious agent that replicates only inside the living cells of other organisms. -Wikipedia

I agree with @AlwaysConfused - I see no reason to close or put this question on hold, it does not seem like a homework question, especially after the OP's recent edits I would suggest the hold be removed.

I don't have a lot of experience in this field to give a full answer, but just for the OP's information, a couple things. First, viruses depend on many key proteins from their hosts. To have any possibility of growing a virus outside a cell, you would have to provide all these proteins, plus the proteins that support/regulate those proteins, a source of ATP, etc. Soon the list of ingredients is essentially just a cell, and (many) cells are fairly easy to grow, so I don't think there is a lot of motivation to finding a way to cultivate a virus outside of a cell, and it would take a lot of work.

Voted to reopen. I was reading a paper from the 30's which claimed to cultivate Vaccinia in the absence of living cells. However a later paper admitted that they couldn't be sure there were no living cells in the media. Of course, given what we now know, contamination with life cells seems most likely.

It depends. Some viruses (like Vaccinia used above) are highly complex and would need a cell to be synthesized (with today's tech). If you take simple viruses, say Poliovirus, you could make the RNA and that alone could be infectious if placed in a cell. This isn't a true virus though, more of a viroid. That being said, take PCV, the single protein will self-assemble and incorporate vDNA, while it might not have been done, this could be theoretically be made in vitro.


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Taking care of Birds: Unwanted species scaring away a less common one from a birdhouse
Near my house, I have set up a birdhouse, which has become home to a pair of Oriental Magpie Robins. They are not a common species in Delhi, India, and are generally shy of human interaction and avian conflict (territory disputes with other species):
However, the birdhouse is constantly visited by a pair of Common Myna. This bird is notorious for being an invasive species and had chased away a pair of Oriental Magpie Robins in the past.
Is there some way for me to get rid of the Mynas without scaring away the Oriental Magpie Robins? The bird is a real menace and I'm afraid it'll push away the Oriental Magpie Robin and other species of smaller birds that visit my locality. It is already considered an invasive species in Australia and South Africa. I don't want to kill the Myna, and trapping is out of the question as well. I just want to scare it off or restrict access to the birdhouse. Is there some way to make the birdhouse and surrounding area more appealing to the Oriental Magpie Robins?

^Oriental Magpie Robin. The darker one is male, the lighter one is female.

^Myna.
Update: The Mynas seem to be guarding the bird house from a distance, since I have been shooing them away. The Oriental Magpie Robin hasn't showed up since.

The best way to foil Mynas is to use an Anti Myna baffle over the nest box. Since Myna always fly directly into the nest box hole, this baffle prevents that while allowing other species to enter the box.


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Which metazoans host anaerobes to aid in digestion? Do any host oxic digestive tracts?
Many metazoans (e.g., mammals, insects, earthworms) have anoxic digestive tracts that are colonized by anaerobic microbes that perform portions of digestion of food for the host.  Some other metazoans (e.g., porifera/sponges) rely on intracellular digestion.
I'm wondering, which metazoan taxa (I suppose we can keep it at phyla level) host digestion that is aided by anaerobic microbes, which do not, and are there any that have digestive tracts that host aerobic microbes instead (though that seems unlikely since they'd likely completely consume the food for themselves)?
We could start by addressing a partial list of the most well described metazoan phyla (plus a few of particular interest to me).  Perhaps no one will have the knowledge/expertise for each of these phyla - in which case we could have a community answer that is built on over time.

porifera- sponges
cnidarea - jellyfish, corals and sea animals
platyhelminthes- flatworms
nematoda- round worms
rotifera- worm-like animals
bryozoa- small aquatic animals
brachiopoda- lamp shells
phoronida- tubeworms
anelida- segmented worms
mollusca- soft bodied animals including chitons, snails
arthropoda- insects and others with hard, segmented bodies
echinodermata- starfish
hemichordata- acorn worms
chordata- primarily vertebrates
placozoa - simplest non-parasitic multi-cellular animals
Ctenophora - comb jellies
tardigrada - water bears
loricifera - tiny shelled sediment dwelling animals

Too broad... should be closed.

I have added a list of specific phyla to make the question more narrow.  It may require multiple answers over some time to fully answer this question and I plan to help by researching and adding answers for some of the phyla.  I could open a separate question for each phyla, but that seems inefficient.


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What, if any, experimental evidence is there that flies rub their legs together in order to clean them?
Everybody's seen a fly rubbing its hands together like Mr Burns. And almost everybody's heard the standard explanation - that it's cleaning itself. Now, this is certainly a very plausible explanation, but has it been demonstrated? I can't find any references to experiments seeking to prove this hypothesis. I'm asking because, not being very familiar with these matters, I'd love to know what methods were used to demonstrate something like this.

A pre-existing answer is linked in the above comment. I admit it doesn't cover the methods used to determine it's really cleansing. However, you cannot ask a fly why its doing something. One can just infer. As a consequence, there's no scientific literature on this afaik.

@Christiaan Well, you could imagine an experiment attempting to prove that the legs are indeed cleaner right after the rubbing ritual. Or you could see if flies rub their legs more frequently in dirty environments than in clean environments.

Oh yes, I can imagine a dozen of experiments, but I can't imagine any funding body to support it

@Christiaan Hey, if there's people irradiating spider webs to track their path through the spider's digestive system, I'm sure someone's doing behavioral experiments on flies.

Haha nice one. In an attempt to answer the linked question I couldn't find anything.


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I get regularly get déjà vu - but I know it's not a memory recall - I always think it's from a dream
My apologies if this is not the right forum for a neuroscientific/psychological question, especially not one coming from personal experience. Please close/move as appropriate :)
Doubtless we're all familar with déjà vu - people invariably describe it as the feeling of recalling their current situation from memory, as though they're repeating something they've experienced in real-life before.
I've regularly had this experience - it happens about once every month or two, the experience never lasts more than 5-10 seconds, and it can be unnerving. However my experience is different from what others always describe: when I'm having an episode I know I'm not re-experiencing something I've done in real-life before, instead I have this feeling that I'm experiencing something I've had in a dream before - a dream premonition, not a memory of real-life. After the experience fades I return to normal and recognize that I have no dream-memories of whatever it is I just experienced - a false feeling of post-hoc premonition.
My father reports the same as well, that he has times where he swears he's "seen this before in a dream" instead of a momentary false memory - he named the experience "breaking a dream" - no-one else seems to using the same terminology as my dad so searching for that online comes up blank. I do see very rare reports online of similar experiences but we "false-dream" deja-vu subjects are definitely in the minority.
I'm curious where my (apparently inherited) ability to slightly discern deja-vu experiences from false memories might come from, and how this "false dream-memory" vs "false real-life memory" difference has a basis in neurology.

Is this probably more suitable for cognitive science (cogsci.stackexchange.com)?

@Chris - nope, it's a personal question - I voted to close because of it here, and will do the same at cogSci.

@Christiaan I suspected that.


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Are surface area or volume conserved during cell division?
I am a student of physics of mathematics with very little knowledge of biology. Nevertheless, I am very keen on biophysics and I'm trying to learn the biological concepts that I need on the way.
I'm preparing now my bachelor thesis (regarding the physics of cell division) and my advisor has recommended me a paper of his where he studies some forces that are relevant in this process.
Under his analysis the constriction of the cell is independent of the area of the cell (the cells constrict on a similar fashion no matter which size they have, the only important parameter is the shape) and he considers several different scenarios. Two of those seemed plausible biologically speaking to me but I don't know if they happen or not in real life. They are to consider the surface of the cell constant during the process or to consider the volume to be constant (during the constriction of the cellular vesicle prior to the division in two new daughter cells).
Are any of these assumptions realistic? Does the area or the volume of the cell undertaking mitosis change drastically during the constriction of the cellular vesicle?

Can you elaborate on what behaviour is assumed to be independent of the cell surface area? The review of the entire paper may be considered too broad, so pick up relevant points and add them in your question. The title also seems broad; can you please narrow it down to a specific point; for e.g. the role of surface tension in cell division etc

Cell area and volume should be measurable (over time) with live cell microscopy. Probably there is some data on this.

@WYSIWYG I have changed the title of the question and added a little explanation. I am interested in the behaviour during the constriction of the cell. Thanks.

What cells do you have in mind? Which organism? Which tissue?

Another PLOS One article gives evidence of change both in volume and in surface area, but it is across mitosis phases. It could still be considered constant during cytokinesis only.
It seems that cell shape and size have important function during mitosis, according to this research. It would be interesting to investigate different models from your advisor's paper (constant maximum radius, volume or area) but starting from different shapes and sizes.


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How long does immunity to influenza last when contracting the disease vs vaccination
The long term efficacy of flu vaccines are well documented, however I cannot seem to find a good source showing how long immunity lasts when contracting the disease.
I suspect it can't be much longer than vaccines since the virus mutates so quickly.

I you feel I can improve my question, please let me know. I don't quite understand why the downvote.

The effect on adaptive immunity are often stronger when contracting the flu than for getting the flu vaccination. The backside of this is that the flu is a quite dangerous disease which could end fatally, so getting the vaccine is always preferrable.
Getting infected by a specific flu strain (or receive a vaccination against it) generates specific immunity against this strain. If it mutates to strong or you get infected with another strain, you will have no immunity (and will have to develop a new immune response.
It seems that immunity against the flu can be livelong (against this strain) after you went through an infection and survived it. There are two studies showing long term response against antigens from the 1918 flu pandemic. The first (summarized in reference 1, the original article is reference 2) shows specific antibodies against the reconstructed haemagglutinin protein (H1) from the 1918 virus strain.
Serum from people born 1915 or before showed specific activity against this virus antigen, even more than 90 years after the infection.
The second study analyzes cross-reactivity of antibodies against the 2009 A/H1N1 pandemic flu strain. Here the cross reactivity of people born before 1930 was the highest - the 1918 strain (with which these people most likely had contact) was also a H1N1 virus. Although these viruses mutated between 1918 und 2009, there is still enough similarity that they are recognized by H1N1 specific antibodies (see reference 2).
A study which compared antibodies responses of people who contracted the 2009 flu against people who where vaccinated against it, showed that the antibody response was more longlasting in the people who got the infection (see reference 3).
So I think it is safe to say that the immune response is stronger after the infection compared to the vaccination, but the vaccination is much safer.
References:

How Long Does Flu Immunity Last?
Neutralizing antibodies derived from the B cells of 1918 influenza
pandemic survivors
Antibody Dynamics of 2009 Influenza A (H1N1) Virus in Infected
Patients and Vaccinated People in China

Thanks for the well thought out reply. I came across the exact same references you did in my preliminary searching. Just to be clear, immunity from influenza is less than a year due to how much it mutates between flu seasons? I know this is true for vaccines, so it stands to reason that it will be similar when contracting the disease.

@niobe Nope, immunity for a certain strain seems to last for a long time, possibly life long. But the strains change from season to season, thats why they need to be adapted. Surface antigens (haemagglutinin and neuraminidase) don't change too much between two seasons, but different strains might get into circulation. Over time they change, this is why we have different strains.

@niobe You may want to have a look at "The Pathology of Influenza Virus Infections".

Perhaps I misspoke, I am aware of antigen drift, which is why I was curious whether immunity to contracting the disease(taking antigen drift into account) is significantly different between the two groups of people as mentioned in the above post. Due to antigen drift, I suspect immunity is seasonal for both groups.


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Are we evolving as fast as the oxygen is depleting?
How much oxygen saturation have we lost in the last 100 years? As oxygen levels dwindle and industry, deforestation,  and population increases, at what year and saturation will the low levels of oxygen become a problem in human development? Would living or sleeping with higher levels of oxygen increase cognitive or physical ability?

Athletes in aerobic sports, e.g., cycling, sometimes live and sleep at lower (rather than higher) levels of oxygen in order to increase their oxygen carrying capacity and improve their physical performance. Particularly high levels of oxygen are actually toxic over moderate time periods.  I'm not sure either of these things are what you're getting at, though.

Good estimates from ice core samples put the decrease in oxygen concentration at 0.7% over the last 800,000 years. At sea level, currently, inspired $P_{O2}$ is (760 mm Hg - 47) * 0.21, approximately 150mm Hg. Human physiology easily adapts to lower $P_{O2}$ levels, with approximately 140 million people living at elevations over 2500 m, with inspired $P_{O2}$ at 108mm Hg, and many permanent human settlements higher than 5000 m, with inspired $P_{O2}$ approximately half what it is at sea level (see West Respiratory Physiology, Ch. 9). A 0.7% decline over 800,000 years isn't going to be much of a challenge.

That is before we had chain saws. I'm looking for more recent numbers and the effects on the human body.+1 for the info though.

@Muze the impact of industry is an increase in certain gases, not a significant decrease in oxygen. The gases that have increased substantially since the industrial revolution, e.g., $CO_2$, $O_3$, $CH_4$ are low percentage gases, but have a significant effect on the temperature of the earth through their interaction with radiant energy. There isn't a significant $O_2$ depleting impact.

So there is a decrease although insignificant. It takes 10 trees to provide enough oxygen for 1 person and if those trees are cut exponentially oxygen supply will also continue to fall. yes?

@Muze Deforestation causes a $CO_2$ problem, not an $O_2$ problem. As you can see from my answer, we have a large excess of $O_2$. $CO_2$, however, is a greenhouse gas, and small absolute increases (which are large relative increases) have significant effects on the biosphere.

@Muze Claims like It takes 10 trees to provide enough oxygen for 1 person would really need a reference. You will note that, if I am not mistaken, while forests are good carbon store, many forest ecosystems do no capture more CO$_2$ than they produce as they've reached their community climax and hence not carbon sink. I would think that such statistics (10 trees to provide enough oxygen for 1 person) hide a much more complex reality and can only be misleading.

@Remi.b reference:  https://space.stackexchange.com/a/26823/18879

@Muze Your reference is a post of yours who itself refers to two posts of yours (one being downvoted and closed)! None of the link support the claim anyway and if they try to do so, they fail to consider the fact that, in an ecosystem, tree die and release the carbon they have accumulated during their lifetime.

@Remi.b some trees can live 100s to 1000s of years old and the carbon is not released in the atmosphere. Not arguing but I did get 200 bonus rep for that link.

Sure but, IMHO, whether they live 1000 years or 2 years, does not change anything that in ecosystems where trees die and others grow up is a carbon storage but not a carbon sink. Anyway... let's no chat further. I have opened the post Does an old growth forest ecosystem produce more oxygen than it consumes? to tackle the question.

@Muze a SE link is not a reliable source to back up a claim on a SE site, no matter how many votes or what bonus rep it has. The original references should be both independent and authoritative or else you run into citogenesis problems :)

Re "10 trees", you're forgetting about the oceans.


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Can a brain dead person recover?
Many times I have heard someone having to pull the plug because the patient was declared brain dead before the body healed fully? Why do they pull the plug without first waiting till the body/brain has a full recovery? What situations if not recoverable would they allow the body to fully heal before pulling the plug?

Hmm... your edit is a different question and kinda breaks the answer. The new answer is "None". Also, "shortly after trauma" is relative. What do you consider "shortly"?

@anongoodnurse revised

No.
Brain death is permanent damage to the brain. Depending on the specific definition, it may refer to either cerebral death or to failure of the brainstem to maintain functions like respiration.
It could be possible for mistakes to be made and for brain death to be declared in a patient who has not actually experienced brain death. However, this is incredibly incredibly rare: zero cases have been reported when appropriate guidelines are followed (Wijdicks et al. 2010). If someone is diagnosed as brain dead after a trauma, the medical staff involved in making that decision are stating that there is effectively no chance for recovery. Brain death is not diagnosed lightly.

Wijdicks, E. F., Varelas, P. N., Gronseth, G. S., & Greer, D. M. (2010). Evidence-based guideline update: determining brain death in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology, 74(23), 1911-1918.

+1. One question, though... I don't know how you can definitively say zero when there aren't detailed studies on serial examinations. I don't disagree with you, I'm just saying that patients aren't kept alive simply to answer the question; that would be prohibitive, and possibly even inhumane.

@anongoodnurse Yeah, I was really just relying on the claim made in the paper I linked. I agree that saying actually zero is probably a bit extreme. There are certainly some cases where patients are kept on life support past brain death (family wishes/disagreements, organ donation, etc), but I agree it would be inhumane to keep folk in that state for a bit just to see if a couple of them recover.

@Bryan Krause answered your question prior to the edit. Your new question is relatively easy to answer.

Why do they pull the plug without first waiting till the body/brain has a full recovery?

Some organs have a high regenerative capacity (you can donate part of your liver and it will mostly grow back), some have a high compensatory ability (you could live with one lung), etc. However, the brain isn't one of those organs.
Until relatively recently, it was thought that the brain had no regenerative ability at all. We now know that to be untrue. Still, compared with most other organs, the brain doesn't "heal" well.
It's one thing to keep a comatose patient alive (e.g. after a bad stroke) to see if time will help. Neurons do form new synapses that allow for a degree of recovery. But most times with a stroke, only part of the brain is involved, and the brain does have compensatory abilities (new synapse formation.)
But brain death is much more than a coma.
When there is so much damage that a patient can be declared to have undergone brain death, people don't recover from that. There isn't any reason to let someone heal all their other organs - or the brain - fully when the one organ that makes us who we are is dead and the only way to stay 'alive' is by artificial means (ventilators, total parenteral nutrition or a g-tube, etc.)

What situations if not recoverable would they allow the body to fully heal before pulling the plug?

Family inability to allow a hospital to "pull the plug" leads to prolonged life support and recovery time for such patients. This is not necessarily good, however. Some patients who were declared brain dead (less rigorous criteria) survived post life support, but none has gone on to become functional (and usually stay in a vegetative - or minimally conscious - state at best.)
Regeneration of Hippocampal Pyramidal Neurons after Ischemic Brain Injury by Recruitment of Endogenous Neural Progenitors

your answer had more info


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Is there any liquid that can replace water?
I understand this is a little futuristic but water freezes and damages cell causing cryostasis yet a reality. Is there any liquid that can be added to the blood synthetic or not that either plants and animals can live on instead of water? Synthetic water?

No. Water is essential both as a solvent and major component of biochemical reactions.
Imagining 'alien life' not based on water, not based on carbon, etc., is only for speculation and science fiction.


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Could Cannabidiol steady a hand?
Can Cannabidiol be used to steady shaky or nervous hand for precision work like surgery?
I have used it for shooting pool/billiards and I'm not sure if it is a placebo or it is helping? but I am more steady.
I have seen where Cannabidiol helps this man with Parkinson's stop shacking.
https://www.youtube.com/watch?v=rAdDdTZuNA8

I'm voting to close this question as off-topic because it is a question of applied medicine. The question would be on-topic on Health.SE.

I'm also voting to close this question as off-topic because it is a question of applied medicine. Please Migrate The question would be on-topic on Health(health.stackexchange.com).

surely you should migrate it rather than close it?

This question is self-help and in its current state it cannot be migrated to Health.

I think this is a fantastic question.
As far as the Parkinson's application, it's definitely within the realm of possible. Taken form a recent review:

Preclinical research in animal models of several movement disorders
  have shown variable evidence for symptomatic benefits but more
  consistently suggest potential neuroprotective effects in several
  animal models of Parkinson’s (PD) and Huntington’s disease (HD).
  Clinical observations and clinical trials of cannabinoid-based
  therapies suggests a possible benefit of cannabinoids for tics and
  probably no benefit for tremor in multiple sclerosis or dyskinesias or
  motor symptoms in PD.

Kluger et al. in Movement Disorder, 2015 (The Therapeutic Potential of Cannabinoids for Movement
Disorders)
As far as every-day hand steadiness, I haven't been able to find any good sources yet. I'll keep reading, and update this if I find anything interesting.


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Can the human body utilize electricity?
In any way could the body store electricity supplied externally?

@MartinKlvana The electron is a subatomic particle, symbol e− or β−, whose electric charge is negative one elementary charge.

electron transfer in mtDNA and nerves (although in nerves, the moving charges are ions, not electrons).

I don't understand your second sentence. It contains no verb. What exactly are you trying to ask here. I don't understand either the purpose or meaning of the picture. Can you clarify this?

@Remi.b I hope that is better.

You seem to be interested in a medical application. Is your question "Can our body sense an electrical current?", "Can our body produce an electrical current?", "Can we cure breast cancer with an electrical current?", "Do different organelles communciate through an electrical current?"etc...

@Remi.b more like if our body has a external consistent charge will our body adapt or has the ability to make use of it

@Remi.b very nice.

I would like this to be migrated to health SE. please

@MartinKlvana Well you might want to discuss this on physics.SE or philosophy.SE but all commonly accepted source of information on the subject suggest that an electron is a particle which carry a charge (which has arbitrarily decided to be negative). An obscure youtube channel with 4 videos, none of them where seen more than 8k won't be a good argument. But let's not further this discussion here, it is not the place.

Not to be a smartass, but do you not consider the mitochondrial electron transport chain to already sort of do that? When we consider that actual movement of electrons to be a step in the conversion of chemical potential in fatty acids and carbohydrates to phosphorylating ADP for later mechanical energy. Just a thought.
Although I'm assuming you mean somehow utilizing a current flow through the body from an outside source.

No, the human body cannot utilize externally applied electricity.  Applying electricity to the body will either have no effect, if the amount is small, or will disrupt normal functions of the body or cause injury if the amount is larger.
An overview of the effects of electricity (for doctors) can be found in "Conduction of Electrical Current to and Through the Human Body: A Review".


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20/20 vision translated to resolution
What resolution and or DPI would a TV or VR headset need to be to equal 20/20 vision? and 20/10? With even the 4K TV it does not seem as sharp as my own vision.

20/20 is a resolution. 4K not (but used wrongly as resolution)

@Charles: no. Number of pixels is not a resolution. It is just used wrongly for computers (and now also on televisions, but TV industry (content side) carefully never used resolution in such context (also because pixels was not a real thing). In any case it is already fading out (number of pixels), because it causes problems, now we are seeing things from much more diverse distances (phone, computer screen, television) as previously. You could use PPI (pixels per inch) as a resolution for screens and paper, or usually it is refereed by lines per angle unit.

@Charles: really. I know about what I'm speaking.You are oversimplifying a complex topic.Really: do not use pixel count as resolution! Do you know that pixel in CSS are not pixel as you mean it (retina display and printing). A pixel on screen has different colours (the subpixels), but on a photographic sensors such subpixels are pixels (so having just one colour ingormation). On printers we use "dots", because dots can be made of different size, and each colour have different resolution. The underling technology (and pixels) should not be taken into account on creating contents.

@Charles  I am interested in both of your answers.

@GiacomoCatenazzi Both point of views has merit and revise the question to be more broad.

Not really on-topic for here, but what sort of video are you playing with your 4K screen? Unless you actually have 4K video, it doesn't matter how many pixels you have. Also, what Giacomo is getting at is that the number of pixels is not the only key - also important is how close you are to the screen. The pixels on a stadium "jumbotron" are going to be huge compared to those on a phone or computer monitor, because they are meant to be viewed from a long distance. There's a big difference if you are up against your TV versus across the room.

Also, 20/20 vision is just a reference to human norms: 20/20 vision means you see an image 20 feet away with similar clarity to how a "normal" human sees an image 20 feet away.

To measure acuity, it's important to have a measure that considers visual space rather than physical world space (it doesn't make any sense to talk about "millimeters" because that says nothing about how far away the object is), so one would normally talk in terms of "degrees or arc" where 360 degrees is a whole field in all directions. Within degrees of arc, you can refer to "arcminutes" which are 1/60th of a degree of arc. If you could see everything in front of you, but nothing behind you, then you have 180 degrees of visual field in both horizontal and vertical dimensions (humans actually have a much smaller visual field than this), or 10,800 minutes of arc.
Your visual acuity greatly depends on where on the retina an image falls; the 'fovea' is the center of the retina where your vision is most sensitive. In the fovea, the maximum acuity is somewhere around 0.5-1.0 minutes of arc (see for example Rossi, E. A., & Roorda, A. (2010). The relationship between visual resolution and cone spacing in the human fovea. Nature neuroscience, 13(2), 156-157.), which corresponds nearly to cone density in the fovea.
A good "rule of thumb" (no pun intended, since we won't be using the thumb here...) is that the width of your fist at arms length is about 10 degrees of arc, your pinky finger is about 1 degree of arc. To get 0.5 arcminute resolution, then, you would need a screen the size of your fist (600 arcminutes) held at arms length to be 1200 pixels wide. Modern cellphones held at a moderate distance likely come near this limit, whereas TVs and monitors typically do not; however, you probably view your phone much closer than arms length and your TV much further.
Realistically, however, pixel counts far below this are sufficient for most scenes, because acuity measured this way is referring to the ability to separate points of light. In real natural vision, we aren't usually separating points of light, but rather organizing visual representations into salient objects, so the actual pixel density required to get a smooth image is less. Pixel limitations are more likely to be apparent when displaying text, since contrast is much higher with text than with natural scenes.

References
Rossi, E. A., & Roorda, A. (2010). The relationship between visual resolution and cone spacing in the human fovea. Nature neuroscience, 13(2), 156-157.


text:
Living potato clock?
Could a potato stay alive and power a clock while growing in the ground?
I know how a potato clock works as a electrochemical cell  and involves chemistry, but I am only interested in a growing plants ability to grow and recover lost compounds, water or otherwise during this process while in the ground.

Side question:
How much power could come from one potato?

Source is in the picture.

I'm voting to close this question as off-topic because this is trivial nonsense.

I’m on the phone so I can’t cut and paste, but read the line in the Tour that states the purpose of SE Biology.

@David is this better?

Better. But I still regard it as off-topic. However others do not. Whether they will give you an answer is another question.

Copper is toxic. The potato may develop a toxic wound at the copper site until it made a barrier there. You should try for yourself, it's such an easy experiment.

@com.prehensible can you make an answer out of that so I can award you the bounty?

Muze, please stop reposting this question. You’ve asked it here before (https://biology.stackexchange.com/questions/69376/potato-power-self-sustaining-medium-using-a-living-potato-plant-possible/69543) and on Physics as well (https://physics.stackexchange.com/questions/277693/a-live-potato-light). If the answers are unsatisfactory to you in those places, please comment or edit your previous q’s rather than reposting duplicates.


text:
How many frames per second do human eyes see?
I observed when a helicopter rotor or fan is spinning the blades blur making it impossible to count the blades, but after a certain speed the blades seem to become visible making it possible to count the blades. Cameras can also do this better.
Do human eyes have a frame rate? What is that called and the most a person can see?
This video in the link shows how these blades seem not to move by timing with the cameras frames rate.
https://www.youtube.com/watch?v=R-IVw8OKjvQ

The term you want is "flicker fusion rate".  For humans, it's about 30 frames per second, though it varies somewhat between individuals: ps://en.wikipedia.org/wiki/Flicker_fusion_threshold

@jamesqf I revised it so your comment can be an answer. Thanks

@BryanKrause TEKKEN?


text:
How much salt [NaCl] is too much in DNA precipitation?
In DNA extractions, how much is too much salt in a CTAB extraction buffer? Protocols hover around 2.5 molar; if you go over this (e.g. 25 molar), will you saturate your solution, and precipitate the DNA too early?
Background:
  Most DNA extraction protocols approximate the following:

~Physical lysis
~Chemical (detergent) lysis
Phase separation (dreaded phenol-chloroform-isoamyl step)
Precipitate, dry

Variants are plentiful, but a common feature of steps 1\2 is inclusion of CTAB and NaCl in the extraction buffer - detergents and salts help to rupture the cell membrane, but (maybe more importantly) CTAB 'selectively'  complexes and precipitates out organic impurities (saccharides, proteins...) while DNA/RNA are left in solution.
For this to work, the net-negative charge of the DNA phosphate (PO4-) backbone needs to be neutralised allowing the DNA to stay in solution: sodium (Na+) ions are attracted to the regular (PO4-) groups, while more irregularly spaced charges*  in proteins etc. associate tightly with CTAB, and 'fall' out of solution: you keep your DNA in the liquid phase and purify, with excess salt washed out at the end using repeated 70% EtOH washes.
Would excess Na+/Cl- effectively level the 'selective' properties of CTAB? 'Salting-Out' the DNA from solution (disrupting the solvation shell) is used in step 4, most often with sodium acetate and 2-propanol: how much salt can be used in Steps 1\2 before the DNA is precipitated out with other organic materials? Are there other considerations (e.g. salts and organic solvents in Step 3)?
First description I've found for this is Zhou (1996), but a really good protocol on it is Wilson (2001).
*: presumably?

What are you afraid of? Did you follow the published protocol? If not, just repeat it and follow the protocol. Ffrom the standpoint of biochemical purification, a cell contains four types of molecules: proteins, lipids, carbohydrates, and nucleic acids.  These last two co-purify through most fractionation steps. As I recall, the CTAB binds to the denatured proteins. and the denatured protein-detergent complex is highly insoluble in the presence of high concentrations of monovalent cations--voila.  RNA can be precipitated by monovalent cations alone, but I don't think DNA can.

Saturated sodium chloride is approximately 6M, making 25M impossible to achieve in water.

@ mdperry my belief was that the Na+ is (also) used to 'cloak' the negative DNA phosphate-group backbone from complexing with CTAB, keeping the DNA in a soluble 'sweet spot': my worry is that too much Na+(Cl-/AcO- etc) will totally disrupt the H-bonding between the solvent and solute, and precipitate the DNA early, at the same stage as the CTAB-protein complexes, though not necessarily for the same reason. Also think you can salt out DNA, but it needs to be cleaned up afterwards.
@MarchHo - Hah, thanks! Challenge accepted.

@incertae_sedis final NaCl concentration in the extraction was increased from 0.5-2M to a dramatic 5M following advice from a colleague and greatly improved DNA yield. Not an answer as such, but suggests not enough NaCl is more likely than too much.


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Surgical vs anatomical neck
What is the significance of differentiating anatomical neck and surgical neck of a bone?
What could be criterias for differentiation?
I found an article here that says fractures to surgical neck are benign, could this be a criteria for differentiation?

Most of the time, I have heard this differentiation in context of Humerus bone only. In that context, have a look at the wiki pages on the anatomical and the surgical necks.
From this, and what I remember from anatomy class, this distinction is more a functional; practical distinction rather than that based on strictly defined criteria. Surgical neck denotes the most commonly fractured region of the bone, and also the region most likely to damage the axillary nerve passing nearby, and hence would have the greatest representation in an orthopedic clinic. The anatomical neck, on the other end, is the classical distinction based on the centers of ossification and the insertion of the capsular ligament of the adjacent shoulder joint, which gives a greater weightage to its origin and to the anatomical relations (insertions, etc).


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My boyfriend and I found this Object on the beach wondering if anyone could help

My boyfriend and I found this object on the beach and need help Identifying it. It looks like a Shark Tooth not for sure. Found in Gulfshore Alabama on the beach. It looked rusty when we found it but after cleaning it up this is what we ended up with. It is 5 1/2" it feels hollow inside.

it could a shark tooth but to get a better guess of what it may be could you post the size and where you found it.
Judging on how it looks it may not be a shark tooth as usually they keep there shape throughout being in the sea.

My best guess is that it is fairly heavily oxidized iron - probably not a tooth, but I can't be sure.

5 1/2" is massive - would have to be Charcharodon megalodon for that size, which would be fossil. Great whites up to 3" apparently.

Looks non biological to me. Definitely not shark tooth

I ran a Metal Detector over it and it Doesn't show up any Metal


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Why is protein turnover necessary or important for cells to function?
Cells constantly create new proteins in order to maintain their normal function, this is called protein turnover.
Why is that? Do the old molecules wear out as time passes, so that they need a replacement?

Clarification: creating new proteins is only part of protein turnover.  A more accurate succinct description would be that protein turnover is the replacement of old proteins with new ones.  The original, unedited version of the question (which focused specifically on new protein creation) makes more sense than the current version.  Turnover is part of the answer to that question.

Biology is an intricate orchestration of chemical reactions and their products. Generally, this fete is accomplished by enzymatic facilitation of certain reactions that would otherwise occur too slowly.
However, "unwanted" reactions occur spontaneously all the time, too. One important mechanism for these reactions is the presence of free radicals causing oxidative stress: reactive molecules are present in cells as a consequence of the energy necessary for metabolism, and these can react with proteins and other cellular components and change their structure. Modified proteins may fold incorrectly and lose their function (or gain harmful function). There is very little that can be done to prevent these reactions from occurring except to clean up afterwards.
Half-lives vary by protein, but for most proteins are measured in the scale of hours (Chen et al, 2016) to a couple days (Boisvert et al, 2012). By constantly degrading and replacing proteins, cells ensure that their proteins are functional and fresh. You might consider this as analogous to performing regular maintenance on a machine like an automobile, using replacement parts as the originals become worn.
Both protein degradation (e.g., via the ubiquitin-proteasome system) and synthesis are highly regulated.

Boisvert, F. M., Ahmad, Y., Gierliński, M., Charrière, F., Lamont, D., Scott, M., ... & Lamond, A. I. (2012). A quantitative spatial proteomics analysis of proteome turnover in human cells. Molecular & Cellular Proteomics, 11(3).
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.

"Half-lives vary by protein, but for most proteins are measured in the scale of hours"Wow that's wild

@AzorAhai-him- Indeed it is, though I want to be careful that I'm not exaggerating things too much. I've added a second reference with a different range of estimates; still hours, but possibly more in the range of tens of hours. Some can be much longer, though; this Biology.SE answer: https://biology.stackexchange.com/a/67698/27148 refers to a couple of those.

Good answer. tl;dr Proteins turn over because they're consumed, modified, or escape homeostasis and require regulation or degradation. Semi-unrelated note, as a tangential rant, how does nobody think to provide keratin/spider silk as an example of a long-lived protein? Keratin (main structural protein composing hair, wool, feathers, nails, horns...) in its native environment can easily and routinely last (tens/hundreds of) thousands of years. If it's a dry place, you'll find it, especially since it's built in bulk. Hooves. Spider silk. Claws. Feathers. Keratin strong.

Still, my haven't-taken-bio-since-HS self would have been off by an order of magnitude

Many aspects of cellular function are related to feedbacks and cycles wherein proteins need to fluctuate in abundance to maintain cellular function.
One example of protein cycling would be cell cycle dynamics. Another would be circadian protein cycling.


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How do you derive steady-state conditions from the open-state differential equation of ion channels?
My books describes this differential equation for the open state of an ion channel:

Where $k$ are the rate constants,
$k_1$ denotes a forward reaction
$k_{-1}$ denotes a reverse reaction in the Markov model

$O$ is the open state, $C$ is the closed state.
According the principle of mass conservation
 $ C + O = 1 $
where $ C $ denotes the closed state
"From here, it can simply shown that under steady-state conditions that $O_{\inf} = \frac{k_1}{k_1 + k_{-1}}$
and the relaxation time constant of the reaction $\tau = \frac{1}{k_1 + k_{-1}} $ "
My question is, how are $O_{\inf}$ and $\tau$ derived?

Is this a homework question? If so it should be tagged as such and you should provide evidence of an attempt to answer it yourself.

@Charles V wasn't important here, so I removed it; C is not the membrane potential its the closed state, such that C+O=1.

You changed V to C and called C "voltage". That's why I explained.

These are really math problems (algebra and basic calculus) rather than biology problems.
Oinf comes from solving algebraically the first equation you posted for steady state: i.e., when dO/dt = 0; just solve for O.
The time constant comes because this is a first-order exponential decay, which you get when you solve an equation (calculate an integral) of the form dO/dT = -lambda * O. The solution to that equation is an exponential decay of the form O(t) = O(0) * exp(-lambda*t)
tau is defined as 1/lambda and gives you the decay rate(relaxation time constant).

Always appreciate explanations for downvotes.

i guess answering bad homework question

@Charles I was trying to give OP some help without doing their homework for them. I understand the style preference, though.


text:
Names for effects of sleep deprivation on the brain & body
When staying awake for a long period (3 or 4 days), some weird phenomena can occur. In my experience, it was always triggered by thinking too deeply and has in other occasions too.
Do these things have names at all?

The brain is a complex dynamic system; if you perturb it outside of its normal functioning parameters (for some examples: severe brain damage, psychadelic drugs, sleep deprivation), odd behavior can result. Note that sleep deprivation for ~2+ weeks kills rats. The rest of your question is too much based on personal health and experience to be on-topic here at Biology.SE.

“Deprivity”? Oh, I see, very clever pun on “depravity” and “deprivation”!

@BryanKrause, I completely disagree. The question of whether there are formal names for the mental changes the OP experienced during sleep deprivation seems to be fine.

@Michael_A Tried to make the question actually about that to keep it on topic, and retracted my close vote.

@BryanKrause, Nice. I thought the original description was a good attempt at describing the phenomena; it's a hard thing to describe. I agree that more words often make discerning the question harder.

During extreme sleep deprivation you can briefly fall asleep, this is known as a microsleep. The disorientation that you experienced can be referred to as  Hypogogia.
Hypogogia covers a range of effects including visual and aural hallucinations as well as having thoughts that are experienced as seeming logical during the microsleep but illogical once you're awake.


text:
How can I determine where meiosis occurs in the life cycle of a plant?
To fill out this diagram with the mitosis, meiosis, and ploidy , we start with the definition that spores are haploid (N).
Based on knowing that as the sperm and eggs are N, the gametophyte is also N (as only fusion can make something go from N to 2N).
Then I know that the link between spores and gametophytes is mitosis, as we go from N to N.
Similiarly, as zygotes are 2N, and spores are N, either the link between zygote to sporophytes OR the link between sporophytes to spores must be meiosis.
Can I figure out at which stage meiosis occurs with this information, or do I need to know more about the definitions of the different parts of the life cycle? How do I know that sporophyte to spores, and not zygote to sporophyte, is Meiosis?
 (Source)

I posted the information from these comments into an answer and edited the original question to try to make it more straightforward, based on what I learned about what your actual questions were. Feel free to revert or re-edit if I have mischaracterized anything; if all is well, you can delete your comments and I will as well to just clean up a bit.

All of these terms are just names for things that existed long before someone named them, and although you can figure out some of the ploidy from the diagram, you need to know the terms/definitions to complete it all.
Sporophytes are just the name for the diploid cells of a plant/algae that reproduces through a haploid life stage called a spore. You could consider the zygote almost like it is a "special sporophyte" from the perspective of ploidy: it's only special because it's the first cell assembled from two haploid cells. All of the other sporophytes are produced from mitosis from either another sporophyte or from the original zygote.
Being diploid is nice because you have two copies of every gene, which is more robust to mutations (while also maintaining genetic diversity for later generations), and, crucially, it lets one organism make a variety of haploid spawn for sexual reproduction.
Maybe you are wondering just about the terms haploid/diploid, and why "2N" vs "N"? The important thing is it isn't just the total number of chromosomes, it's the number of COPIES of each chromosome: with N you have just 1 of each, with 2N you have two of each. The important thing is that they are homologous, it doesn't matter if N is 1 or 2 or 40.


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Do voltage-gated channels in a neuron use ATP
I have a question about action potentials in a neuron.
Do voltage-gated sodium and potassium channels use ATP? I mean when they are closed or when they want to open the gate, do they use ATP?

No, they change conformation in response to voltage. Wikipedia has some general discussion of the gating process, as would any basic neuroscience textbook.
The primary energy (ATP) cost of neurotransmission is in establishing ion concentration gradients, via the sodium/potassium ATPase. You can think of this as a special case of secondary active transport, where the energy costs are in establishing a gradient that is then used for a later process which does not cost any direct energy.

Learning and memory (synaptic weight matrices) are mediated, in part, by the concentration of voltage-gated sodium channels at the neuron’s axon initial segment. The more voltage-gated sodium channels, the more efficacious is the transformation of a neuron’s collective synaptic input potentials into output action potentials. Those voltage-gated sodium channels, dendritic spines, ion gradients, and synapses are continually be built up and broken down depending on the learning needs of the animal. While it is true that the Na, K, and Ca flow down electrochemical gradients when depolarization opens up the voltage-gated ion channels (and don’t use much ATP/energy at that instant), there is an immense expenditure of ATP/energy in the prefatory synthesis of protein, degradation of protein, and pumping ions against electrochemical gradients in order to establish the membrane potentials in the first place. Source: Lou, L. “Principles of Neurobiology” Chapter 10

It's typically ligand-gated channels that change concentration with learning and memory. Voltage-gated channels at the axon initial segment can regulate the transfer function, yes, but this affects all inputs to a cell rather than affecting them directly. In any case, this seems mostly irrelevant to the question asked.


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Arteries used for inserting catheter
For catheter purpose, femoral and subclavian arteries are mostly used as starting point. Why? Are there other arteries which are used for the purpose?

What research have you done? What aspect you didn't understand?

research - "For catheter purpose, femoral and subclavian arteries are mostly used as starting point."

What have you searched regarding your question?

depends on the purpose that you're talking about... we insert catheters for hemodynamic monitoring into the radial, brachial, femoral arteries. For other percutaneous methods, other arteries could be accessed, but less commonly - depends on what purposes your talking about

Those arteries are (a) big enough for the catheters, (b) superficial enough (close enough to the surface of the skin) for catheterization. It would be quite a challenge to use the renal arteries, for a ridiculous example. There is also less of a risk of embolization than using an artery like the carotid, where embolism can cause stroke, which would be quite serious. An embolism in an arm or leg could be painful and cause damage, but unless it is massive it isn't going to significantly affect the patient over the long term.
Also note that those are fairly special cases of catheterization, such as when doing percutaneous interventional techniques targeting the peripheral or coronary arteries. Those approaches use fairly large devices so you need a large vessel, and you need to be in the portion of the vasculature that you are targeting (i.e., you can't access those targets through a vein). As @VanceLAlbaugh mentioned in a comment, other arteries are targeted for other purposes. And overall venous catheterization is much more common than arterial, such as when an IV line is established to deliver fluids/medicines.


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Why do V_Na and V_K stay unchanged in Hodgkin-Huxley model?
In the Hodgkin-Huxley model, ionic current $i_\mathrm{Na}$ and $i_\mathrm{K}$ are given by
$$
i_\mathrm{Na}=g_\mathrm{Na}(V_\mathrm{m}-V_\mathrm{Na})\\
i_\mathrm{K}=g_\mathrm{K}(V_\mathrm{m}-V_\mathrm{K}),
$$
where $V_\mathrm{Na}$ and $V_\mathrm{K}$ are the equilibrium potential, and are kept the same during the burst of action potential:
$$
V_\mathrm{Na}=\frac{RT}{F}\ln\mathrm{\frac{[Na^+]_o}{[Na^+]_i}}=35~\mathrm{mV},\\ V_\mathrm{K}=\frac{RT}{F}\ln\mathrm{\frac{[K^+]_o}{[K^+]_i}}=-85~\mathrm{mV}
$$
This means $\mathrm{[Na^+]_o,~[Na^+]_i,~[K^+]_o,~[K^+]_i}$ are all constants, which is really confusing. In my opinion, the inward/outward current of sodium/potassium ions should definitely change the concentrations of Na+ and K+.
Well, it makes sense that $\mathrm{[Na^+]_o}$ and $\mathrm{[K^+]_i}$ can hardly change because they are large enough compared with the lost ions into the regions with fewer ion concentrations. Then what about $\mathrm{[Na^+]_i}$ and $\mathrm{[K^+]_o}$? They are so small that even very a few ions added to them can change them a lot.
For example, $\mathrm{[K^+]_i}=90~\mathrm{mM}$ and $\mathrm{[K^+]_i}=3~\mathrm{mM}$. If the potassium current leads to a change of $\mathrm{1~mM~[K^+]}$, now $\mathrm{[K^+]_i}=89~\mathrm{mM}$ and $\mathrm{[K^+]_i}=4~\mathrm{mM}$. $\mathrm{[K^+]_i}$ changes by 1.1% which can be neglected, but $\mathrm{[K^+]_o}$ changes by 33.3%, which cannot be neglected. Also, the equilibrium potential of potassium now becomes 25*ln(4/89)=-78 mV! This really changes a lot. How can we ignore it?
Moreover, in the Quantitative Model of Gastric Smooth Muscle Cellular Activation of Corrias and Buist (Annals of Biomedical Engineering, Vol. 35, No. 9, 2007), both $V_\mathrm{Ca}$ and $\mathrm{[Ca^{2+}]_i}$ does change during the burst of action potential as follows:
$$
\frac{d[\mathrm{Ca}]_i}{d t}=-\frac{I_{\mathrm{caL}}+I_{\mathrm{caT}}}{2 * F * V_c}-I_{\mathrm{CaExt}}.
$$
But they also ignored the change of $\mathrm{[Na^+]_i}$ and $\mathrm{[K^+]_o}$. Hmmm, really confsuing.

As you've figured out, the reversal potentials don't change because they're assuming the concentrations don't change. Even relative to $\mathrm{[Na^+]_o}$ and $\mathrm{[K^+]_i}$ the number of ions that move is small (e.g., see this previous Q&A: Ambiguity about the relation between membrane potential and concentration gradient in neuron cells - the squid giant axon isn't quite as efficient as a mammalian neuron but it's not so bad, either): 1/100,000th of the internal potassium is still on the order of 1/10,000th to 1/1,000th relative to the outside. Changing the concentrations by 0.1% isn't going to appreciably change the reversal potential. The example you give of a 1 mM change is far, far greater than what occurs with typical neuronal activity.
Of course, over a longer time scale there would be changes in concentrations, but those changes aren't observed as long as the sodium-potassium pump is active. The pump is working all the time to maintain the concentration gradients observed in neurons, and if you were to disable it the concentrations would eventually equalize across the membrane.
Calcium is in much lower concentrations than either sodium or potassium. It's also buffered heavily intracellularly so that the "observed" calcium concentration is absolutely miniscule: free calcium ions are important in signaling, but they are very quickly bound strongly by various chelating molecules inside the cell. Inside the cell, just a few hundred or thousand calcium ions make a big difference.
There's a bit of a famous quote/aphorism by statistician George Box and others that goes something like "All models are wrong, but some are useful" - so, that's what you're seeing here. Is the HH model absolutely complete to cover all aspects of neuronal function? No, of course not, but if it were it would be missing way more than just the changes in concentration of the ions involved. For the data that HH were fitting, and for many other circumstances involving neurotransmission, this model does well enough. It certainly does well enough for learning, describing, and teaching the basic mechanisms that are critical to neurophysiology. Including more of the total system would require many more free parameters without much improvement to the model.
In some other circumstances, such as hypoxia where the sodium-potassium pump does not function well, or seizures where the level of activity is extremely high and the extracellular space can get flooded with potassium, it may become more important to account for changing sodium and potassium concentrations. For more typical cases, they can usually be ignored and assumed to be held near enough to constant both inside and out thanks to the sodium-potassium pump.


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Why does Stereology use Systematic Random Sampling?
I am a student of Neuroscience and in all my textbooks and lecture notes it is written that in Stereology, Systematic random sampling (SRS) is used to obtain sections.
Why it's that and not any other type of sampling? For example, why do we not use completely random sampling? What are the advantages of SRS over any other type of sampling when applied to stereology?

I really like questions like this, thank you! I am glad you are curious about why approaches like this are used - I strongly recommend that all students try to think critically about techniques, you can learn a lot from this approach!

Systematic sampling refers to a method where all samples have an equal probability of being chosen but the spacing between samples is constant. That is, although each individual section is equally likely to be chosen, the combination of samples is not. The Wikipedia article on systematic sampling provides a good overview.
Stereology refers to the analysis of a three-dimensional structure using two-dimensional slices. Such an approach is common with histological techniques. A block of tissue is sliced into thin sections that allow for examination of the tissue with light microscopy, usually with the aid of stains.
If you sampled purely randomly, by chance, you are likely to obtain "gaps" in your analysis by random chance. For example, imagine you section a 3mm block into 40um sections. This process gives you 75 sections. It is too time-consuming to analyze all 75 sections, so you want to choose just 15 of them.
Let's try generating 15 random numbers from 1 to 75 and look at the maximum gap. I do this by taking the first 15 numbers of a random permutation of 1 to 75. In MATLAB, one can do: x=randperm(75,15), max(diff(x));
Here are some results:
23    26    33    34    35    37    44    54    55    58    60    69    72    73    74

Max diff: 10
12    14    15    16    17    20    22    27    28    34    44    47    58    59    73

Max diff: 14
 8    14    15    18    19    20    29    32    40    41    47    67    70    71    72

Max diff: 20
 3     7    16    19    30    32    33    34    38    39    50    57    61    65    75

Max diff: 11
 3     7    17    18    21    26    29    37    42    46    49    52    60    61    69

Max diff: 10
If we were to instead use systematic sampling, the difference between sampled sections would be fixed at 5: you skip 4 sections to get 15 evenly spaced sections out of 75 total. But with purely random sampling, the largest gaps are bigger, sometimes much bigger! 20 skipped sections means there is a 800um gap with no data! Even worse, I noticed later that in the first draw, the lowest number was 23! So the first 22 sections are completely omitted from analysis! There can be major morphological changes and entire brain nuclei missed within a gap that size, whereas 100um gaps are no problem.
I didn't print out the minimum gaps, but you can look at my examples to see the other side of this problem: in the first set, numbers 33, 34, 35 and 72, 73, 74 are right in sequence! There is likely little or no morphological difference on those short intervals and yet with random sampling one can waste time analyzing those adjacent slices. Because these draws are completely random, you can notice similar adjacent stretches in all of these random draws, even though I made no effort to select particular examples: these are just the first 5 results I got from MATLAB.
References

Gundersen, H. J. G., & Jensen, E. B. (1987). The efficiency of systematic sampling in stereology and its prediction. Journal of microscopy, 147(3), 229-263.
Gundersen, H. J. G., Jensen, E. B. V., Kieu, K., & Nielsen, J. (1999). The efficiency of systematic sampling in stereology—reconsidered. Journal of microscopy, 193(3), 199-211.


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Question About Molecular Weight
In Lehninger's Principle of Biochemistry Pg. $14$, this is the definition for molecular weight (relative molecular mass):

The molecular weight of a substance is defined as the ratio of the
mass of a molecule of that substance to one-twelfth the mass of
carbon- $12$ ($12$C). Since $M_r$ is a ratio, it is dimensionless—it
has no associated units.

What I do not understand is how we find the mass of the molecule in the beginning. What unit would we use?

@user1136 The phrase "molecular weight" may be frowned on, but I doubt it's ever going to go away unless all the reagent makers get on board. I don't think I've ever seen a protein standard marketed as a "molecular mass marker"...

@user1136 I agree with you that the most precise term should be used, I just wanted to make the point that there is a lot of historical weight (so to speak) on the term "molecular weight", and I don't think its usage will decrease until reagent makers get on board.

I voted to close this question as off-topic as it is a general chemistry question.

The mass of a biological molecule is evaluated by the process of Mass Spectrometry (specifically MS/MS or MALDI-TOF). These are an improved version of Mass Spectrometry(MS) and results from the works of physical chemists.In a nutshell, you can ionize the molecule. It dissociates into several ionized particles. Then subject them to a magnetic field and an electrical field at the same time.
The ionized particles take a curved route while moving , and the amount of curve depends on m/q of molecule ( mass of particle (in kg) and charge of it)
see
https://en.wikipedia.org/wiki/Mass_spectrometry
Molecular weight is dimensionless indeed. However one may add Dalton/amu/u "False" physical units for better understanding.
The best other example in physics is radians. Angles are defined in radians in physics. But they are dimensionless.
In Circular motion , we have these formula :
$ v = \omega \times r$
$\theta = \omega \times t$
see:
this
unit of $v$ is (meter per second) and unit of $r$ is (meter). therefore the unit of $\omega$  is  $s^{-1}$ .
unit of $\omega$ is $s^{-1} $ while the unit of $t$ is $s$.
So $\theta$ is dimensionless although we describe it as radians for better understanding


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Why does NaCl react differently with a boiled potato and with a raw one
Well my question is based on this question down below.

For those who don't speak german:
You have two potato slices one of them is boiled the other one is just raw.
Now you scatter some salt over both surfaces of the two different slices and wait about one hour.
After the time is over the salt on one potato isn't in his crystalline formation anymore.
So my question is why are behaving both slices different?

My guess is that the carbohydrates ( Starch ) reposition and the starchcores bind with H2O.
So the H2O binds with the NaCl?

I would really enjoy it when somebody could tell me the chemical reasons why this happens.

I think it should be in Chemistry stack exchange instead of biology.

@AlwaysConfused seems far more likely to me that the boiled potato simply doesn't have enough water to melt the salt.

Maybe this passage is referring to this experiment?
The key missing from your description is that each potato is placed in water. When the cells are intact (unboiled), this causes water to flow into and out of the cells via osmosis: into the cells from the tray of water, and out from the cells into the salt. Once the cells are destroyed via boiling, there are no intact membranes to cross to osmosis does not occur and the salt remains undisturbed.

Well sorry if I'm confusing you but I guess you're always confused:P
For those who are saying I forgot about the point that the potatoes were placed in water before the salt was scattered. Well that is exactly the problem just one were placed in water and got boiled. The other one was never getting in touch with water. And I don't know if it's the raw or boiled one which changes the crystalline formation.
The answer that the boiling destroys the cells and also the membranes which are essentially needed for the osmosis causes the behavior that the boiled let the salt untouched seems legit.


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Why is trypsin digestion required for proteomic studies?
I know that trypsin is used for proteomic studies, but I do not understand why trypsin digestion is necessary/important.

Welcome to SE biology. Could you edit your question to make it clearer. Proteomics is not a synonym for mass spectrometry. I think you want to ask Why is tryptic digestion used prior to mass spectrometry?

Trypsin digestion allows you to cut proteins into smaller polypeptides, masses of which can be determined by mass spectrometry and then translated back into possible amino acid sequences. Trypsin cleaves after specific amino acids. Altogether, this allows you to identify proteins.


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Is it unusual for a child to be diagnosed with diabetes?
Recently, I came to know that a boy in my town who is 6 years old is diabetic and many people were shocked from this news.

Short Answer
Type 1 diabetes is commonly diagnosed in children; type 2 diabetes is more common overall and is much less likely to be diagnosed in children, though possible.
Longer Answer
Type 1 diabetes is caused by damage to the pancreas and depends on environmental and genetic causes, most often leading to autoimmune loss of the insulin-producing beta cells in the pancreas. Type 1 diabetes occurs because insulin levels themselves are low. It commonly begins in childhood, and is also sometimes referred to as "juvenile diabetes" although it lasts life-long. Type 1 diabetics often take insulin to replace the insulin they are not producing.
Type 2 diabetes, by contrast, is caused by reduced insulin sensitivity and develops over time (lack of insulin can also eventually occur). Obesity and other lifestyle factors are strong influences on the development of type 2 diabetes, though genetics can also play a role. Type 2 diabetes is most often diagnosed in adults (and is also referred to as adult-onset diabetes, though it is also possible to occur in children), increases with age, and is overall more prevalent than type 1 diabetes, so this is likely where your community's surprise comes from.

Your overall answer is correct, but I'd add that type 2 diabetes runs in families, while type 1 does not. There are MHC associations with type 1 because it is autoimmune in origin, but clinically, we don't think of type 1 diabetes as a genetic disease.

I focused on the first phrase (type 1 diabetes is caused by genetic factors), but on looking again, you should probably correct the rest of the sentence. The specific cause of type 1 diabetes is usually known. It is autoimmune destruction of islet cells. I'd have to look it up again to be sure, but I believe anti islet cell antibodies are identified in almost all cases.

If you are going to edit, I recommend directly answering the question instead of posting information for the asker to infer from.

@DeNovo My understanding is that type 1 diabetes has quite a high heritability, and concurrence in families is rare only because the disease itself is rare, i.e., the heritable factors are a risk rather than a clear cause. I can certainly try to reference better if this is unclear or controversial, I wasn't realizing that it was.

@Cell If you are referring to my edit of the question title, I did so due to the body of the question which in my experience is usually a better marker for what new question-askers are going for here at biology.SE. I've added a more clear direct answer, however.

That's just the way it was taught in medical school (though that was a while ago)-- family history is more important for type 2 than type 1, so it was jarring for me to see type 1 described as a genetic (rather than autoimmune) disease, with the heritable component of type 2 downplayed. I'd appreciate some better sourcing if you want to contrast them in this way. Though I'm not sure you need it for the answer. Genetic doesn't necessarily mean "appears in childhood", as I'm sure you understand.

A quick search brought me to this review on type 2 and this one on type 1. They're both highly heritable, but when you compare apples to apples, it looks like what I was taught in medical school still holds. Type 2 is more heritable than type 1.

@DeNovo The twin concordance is higher in type 2 because prevalence is higher, but it doesn't really look like type 2 is more heritable biologically, at best they are similar. That review on type 2 also says that a lot of the type 2 heritability is explained by heritability of obesity. I don't disagree that what you learned clinically is relevant clinically, though.

If obesity mediates the heritability of T2DM, it doesn't make T2DM less heritable. Obesity isn't just associated with T2DM, it is on the causal pathway. This means obesity isn't a confounder.  You say T1DM is caused by genetic factors and T2DM is caused by environmental factors, though genetics can also play a role. I don't see any support for that contrast, and it is in conflict with standard teaching on the pathogenesis of the two diseases. If you want to make that argument (which you don't need to do in order to answer the question), I think you should include some non wikipedia sources.

@DeNovo As you point out, since it isn't necessary to answer the question, I can make the contrast less obvious.


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When is the sex of a human not determined by their chromosomes?
This might sound like a silly question, but what chromosomes determine whether a human is born a boy or a girl? I ask this because I got https://embryo.asu.edu/pages/sex-determination-humans when googling the subject and it contains the word "typically" in places I did not expect. For example:

Humans typically develop as either male or female

Humans who inherit two X chromosomes typically develop as females, while humans with one X and one Y chromosome typically develop as males.

Because females tend to only have X chromosomes, the egg cells that they produce typically carry an X chromosome

Is this a form of political correctness, or are there legitimate cases that justify the insertion of the word typically? I'm genuinely curious what these exceptional cases might be.

To answer points 1 and 2:
People born karyotypically male (XY) with complete androgen insensitivity syndrome (AIS), can be born without developed male genitals. People with a certain set of sex chromosomes develop in varying different ways.
To answer point three: An egg cell will indeed carry a single X chromosome in most cases, however, there are situations where an egg cell can carry two X chromosomes. If an egg cell containing two X chromosomes is fertilized with a sperm containing a Y chromosome then this could lead to XXY chromosomes — Klinefelter syndrome.
Side notes:
For those interested in the impact of social standards regarding this syndrome, there is a good interview with a Dutch person with AIS. (One can set the translated captions to most languages.)
You can find information on the occurrence rate of intersex here:
Intersex Society of North America

Very interesting! Thank you very much.

There is a a whole mess of inhibitors and activators proteins that need to be triggered for typical sexual development, a mutation or error in any one can lead to atypical results even if they have typical chromosomes. A graphical overview is below. You may note than several factors are common to both sexes. Atypical can range from just malformation of genitals to full on sex reversal. XY female and XX male exist.  Then you have all the atypical chromosome combinations, Xo, XXX, XYY, XXYY, ect. A full breakdown of most the known options (as of 2016) can be found here. And that's just the gross physical manifestations, the brain has largely separate pathways for sex determined development, meaning an alteration of those pathways can lead to what is essentially a male brain in a female body and vice versa.

https://www.semanticscholar.org/paper/Sry-and-SoxE-genes%3A-How-they-participate-in-sex-and-She-Yang/3860ee65052aebecc48a85a79a36221160458b30
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5866176/


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Hypothetical violation of independence assumption for linear models
Let's say I have measured the abscisic acid content (could be any metabolite really) of 10 individual plants which we can consider biologically independent. Then I repeat that measurement for all 10 plants on 15 different days over the course of a year. I then want to correlate, with a linear regression model, the values of abscisic acid with the amount of rainfall (from publicly available regional data, say) on each of those days. What is statistically appropriate?
Firstly, I believe that a mixed model should be used, with individual plant as a random effect, to account for the fact that I am repeatedly measuring the same plant over time.
On top of that, am I not also in danger of pseudo-replication from the fact that my rainfall has only been measured once for all 10 abscisic acid measurements (i.e. the abscisic acid vs rainfall measurements are not really independent on each day either)?

Observations are assumed to be independent, not predictors. For example, if you were doing some chemical fertilizer treatment, you'd probably not apply a random chemical or random dose of chemical to each plant, you'd most often choose a small number of doses, and have far fewer values of the predictor than you have observations.
But, I do think you've identified a potential issue here, it's just that it isn't about repetition in the rainfall measurements, it's about additional repetition besides rainfall in your observations: there are going to be a lot of other environmental variables, besides the one you measured, that are the same for all the plants because you're measuring them on the same day, and that's potentially going to introduce correlations in same-day measurements.
It probably makes sense to account for that using a random effect for observation day, in addition to a random effect for each plant.
That approach may not work well if there are other specific factors that have a substantial impact (you should try to measure and account for those directly, instead), or if it's not really right to make the choice of day as a "random" feature, for example if there are seasonal variations you may need to track time explicitly. It all depends on what you know about the system you're studying.