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Is Chemiosmosis a hypothesis or a theory?
I was trying to find out whether chemiosmosis is a hypothesis or a theory. Naturally, I first searched on Wikipedia, but the article on chemiosmosis uses both the words, which is confusing.

The chemiosmotic theory
Peter D. Mitchell proposed the chemiosmotic hypothesis in 1961. The theory suggests essentially...

...the weight of evidence began to favor the chemiosmotic hypothesis, and in 1978 Peter Mitchell was awarded...

In chemiosmotic theory transmembrane ATP synthases are...

Then I found several papers; some of them use the word hypothesis like this one, this one and several others, but few others use the word theory like this one, and this one.
To my knowledge, a hypothesis is an educated guess based on certain data that acts as a foundation for further investigation while a theory explains a natural phenomenon that is validated through observation and experimentation but I am not aware of any experiments conducted by scientists to test this?
In summary:
Is Chemiosmosis a hypothesis or a theory, and what experiment has been performed to test it?

Edited your question so that now it's not obvious that it's actually two ;-)

I have now edited the Wikipedia page, changing theory to hypothesis. We'll see how long it lasts before someone tries to revert it, and what the eventual outcome may be. In part I did this to demonstrate that Wikipedia entries can be edited by anyone (unless they are politically controversial etc.) and that they are a communal effort with no single formal editor. You cannot assume that they are correct, only that they are correctable.

Preamble
Although there is a case for closing this question (it is two questions, the first of which is more linguistics, logic or philosophy of science, and the second well-covered in text books) I have chosen to answer it, mainly because neither of the terms hypothesis or theory describe the current status of the proposal (the neutral description I shall employ initially). I have restructured my original answer putting the science first, and providing more information on this.
Mitchell’s Proposal
As the title of his original 1961 Nature paper makes clear (“Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism”) Mitchell was addressing the following question: How is the free energy released from the electron transport chain — involved in the oxidation of NADH and FADH2 by oxygen — used to phosphorylate ADP to ATP.
At that time it was assumed that this was by a mechanism in which the energy was used to generate a chemical compound, X~P, containing a phosphate bond with a high free energy of hydrolysis, which could be used to phosphorylate ADP to ATP. (This was influenced by the ‘substrate-level’ phosphorylation occurring in glycolysis.) In brief, Mitchell proposed that the phosphorylation did not involve any compound, X~P, but was catalysed by an ATP synthase enzyme powered by an electrical gradient, established across the membrane in which the electron transport chain resided.
Mitchell proposed a possible mechanism for oxidative phosphorylation in terms of conventional physics and chemistry. Just as the postulated X~P, had not been identified, neither had the components of his proposed chemi-osmotic mechanism. The paper focused on its quantitative feasibility (making it challenging reading for many biological scientists), although it did also argue that the idea was consistent with a series of experimental observations that were difficult to explain in terms of substrate-level phosphorylation.
It was a hypothesis
Regardless of the interpretation of dictionary definitions, considered below, it was a hypothesis because that was the word Mitchell used in the original paper, cited above, a paper in which the word theory does not occur.
As well as misquoting history, it would seem presumptuous to use different terms to refer to the proposal of the original author, a proposal which resulted in his award of the Nobel Prize.
It is a fact
The mechanism of oxidative phosphorylation has now been explored in great detail and the general features of Mitchell’s hypothesis have been generally validated. It can be considered as much a fact as any other in our general conception of cellular biochemistry.
The famous experiment that resulted in widespread acceptance of the hypothesis was the so-called acid-bath experiment of Uribe and Jagendorf. In this experiment ATP was generated in the dark and without electron transport by loading the inner space of the grana disk membranes of spinach chloroplasts with protons.
More recently the structures of all the proteins involved in the chemiosmotic mechanism have now been determined, including that of the ATP synthase, the molecular machine which uses the electrochemical gradient to phosphorylate ADP to ATP. and the components of the electron transport chain.
Dictionaries
Merriam–Webster, on-line, is quite dogmatic about the difference between the words hypothesis and theory:

A hypothesis is an assumption made before any research has been done.
It is formed so that it can be tested to see if it might be true. A
theory is a principle formed to explain the things already shown in
data. Because of the rigors of experiment and control, it is much more
likely that a theory will be true than a hypothesis.

But is this dogmatism justified, and how does it apply to the current problem? Mitchell’s proposal was made to be tested (as in a hypothesis) but it was intended to explain the observed phenomenon (as in a theory) of oxidative phosphorylation.
An extensive article in Wikipedia begins with a more modest statement:

A hypothesis (plural hypotheses) is a proposed explanation for a
phenomenon.

And chemi-osmosis is a proposed explanation for the phenomenon of ATP synthesis in double-membrane systems; so by this token Mitchell’s choice of words seems justified.
Major dictionaries record how words are or were used in practice. In some contexts there are sharp distinctions in usage of particular words, where in others the same words are used interchangeably. In modern biological science, unlike philosophy, logic or the numerical sciences, laws, theories and hypotheses are generally of no great concern, and the writers quoted may merely feel that the word ‘theory’ (‘Einstein’s’ theory, ‘Darwin’s theory’) has more gravitas than ‘hypothesis’, a word they perhaps use to describe ideas about relatively humble scientific problems of their own.
…or they may just find it easier to spell.

Understood, I don't think I possibly know how to merge my two questions now, but I'll sure keep that point in mind for my future questions. Again, thanks!

also reg the textbook i'll try to get my hands on one

Revised my answer. Principle the same, but more information on theory and evidence for it.


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Does cytoplasmic streaming exert a force on the cytoskeleton itself?
In plant cells, cytoplasmic streaming is though to be driven by the force generated from active transport of myosin-cargo complexes along actin highways. Does this force also act on the actin filaments themselves? Does it contribute to the movemement of the cargo along these filaments?

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How can we use the number of crossovers per chromosome to calculate the recombination rate in cM / Mb?
I was reading a paper titled "Tetrad analysis in plants and fungi finds large differences in gene conversion rates but no GC bias" (2018). According to this paper:
"The between-species differences in CO rates reflect in part the fact that each chromosome needs at least one chiasmata. Indeed, the CO rates are more uniform when expressed as CO events per chromosome with about an order of magnitude difference in cM Mb-1 per chromosome: from ~5.3 COs per chromosome in yeast (= 22 cM Mb-1 per chromosome, N = 16) to ~2.3 COs per chromosome in Neurospora (= 2.8 cM Mb-1 per chromosome, N = 7), to ~2.2 COs per chromosome in Arabidopsis (= 0.9 cM Mb-1 per chromosome, N = 5) to ~1.4 COs per chromosome in Chlamydomonas (= 0.7 cM Mb-1 per chromosome, N = 17)."
Here, the authors give 1) the number of crossovers per chromosome in each of these four species and 2) the equivalent recombination rate in units of cM / Mb. However, I don't understand how the conversion was reached in each case.
Take Chlamydomonas reinhardtii for example, with 1.4 COs per chromosome. There are 17 chromosomes, so that's 23.8 total crossover events. (Roughly agrees with Table 1.) The whole genome is ~110 Mb, so that's 0.216 CO / Mb. And ... I am unsure how to proceed. It's just not clear to me how to complete the conversion for any of these organisms. How can I calculate the recombination rate in cM / Mb, as the authors of this paper did, from the number of crossover events?

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What is the evidence for cognition being mainly confined to the brain?
We believe that the processes of cognition are mainly confined to the brain.
What is the evidence for that?
I understand that the brain shows increased oxygen saturation in fMRI scans while thinking intensely. Therefore, we can conclude that brain plays a role in cognition. But how do we conclude that the rest of the body plays a negligible role in it?
In other words, how can we be certain that the brain's role in cognition is not a supportive one rather than an almost exclusive one?
I know that there is enough evidence for brain having a role in cognition, however my curiosity is mainly that why do we confine it to the brain alone? In other words, how are we certain that cognition is not spread outside the brain?

I think tetraplegics generally have no troubles with cognition, so we can rule out all four limbs. There are people living without stomach, half of lungs, without kidneys, with severly shorter intestines, smaller liver, no eyes, no tongue, non-functional ears, heart-transplants ... yet all of them (can) have normal cognition ... However, even a tiny damage to the brain can lead to significant cognitive disabilities. So ... which organ do you propose as an alternative center for cognition? :)

By studying countless insults to the brain, all aspects of cognition have been identified, even pinpointed to particular parts of the brain, not only in humans but in other animals as well. We know where memory is, where speech centers/understanding speech is located, where pleasure is perceived, etc. Dogs trained to be still in MRI machines exhibit the same patterns in the same places with certain stimuli. A heart transplant (or other) doesn't make the recipient think like the donor. Look up fMRI; that maps cognition as it happens.

@Domen Thank you for your comment. That is definitely a good piece of evidence.

@vkehayas Yes, thank you. Actually, my question arose out of similar contemplations.

@anongoodnurse Thank you for your comment. Insults, injuries, and fMRI do establish that brain has a role in cognition. What I wondered was how can we be sure that it has almost exclusive role, rather than a supportive one?

@Domen Could you please add your comment as an answer? It did help me understand the reasoning behind the idea.

I have extremely good "gut intuition"... which is found in the brain. What kind of cognition is not found in the brain? What are you imagining any other organ can do in terms of cognition? Which organ? The liver? The heart? You've been given plenty of replies.

@vkehayas I would not say a brain in a jar cannot cognate, it is just very difficult to demonstrate cognition. Brain in jars for animals when connected to circuitry can control robots. https://www.science.org/content/article/lamprey-brain-drives-robot#:~:text=Through%20trial%20and%20error%2C%20the,or%20circle%20patterns%2C%20Fleming%20says.

Also, people that go into comas and brain death have great vital signs from all of their body, although we can see from their brain activity that it is different and causing the coma. brain death: https://www.life-source.org/latest/what-is-the-difference-between-a-coma-and-brain-death/

Who said cognition was confined to the brain (I mean, before you posted the question here)? Definitions probably vary somewhat, but most seem to include experience and sensory information as inherent components of cognition, so I'm just curious where that opening statement came from. Particularly the word "confined." This question might actually be better suited for Philosophy.

The single best evidence is injury and deformity.
You can lose any other part of the body without impairing cognition but brain damage especially damage to specific parts of the brain alter or damage cognition. Losing a foot or a kidney or an eye does not suddenly make you unable to speak, but damage to the language center of the brain does. Cataloging the effects of damage to different parts of the brain has actually given a fairly decent map of what different parts of the brain do before we started scanning active brains.
https://uwmsktc.washington.edu/sites/uwmsktc/files/files/TBI_cognitive.pdf
https://www.biausa.org/brain-injury/about-brain-injury/basics/function-of-the-brain
Animal brain removed from their bodies and connected to circuitry can learn.
As for how can we be certain, we can't, that's not how science works. We can say it is extremely likely given existing evidence and there is no evidence to the contrary, to the point it can be safely assumed, but science does not deal in absolute certainty.

Thank you. The links were educative to me.

Degeneration of the muscles controlling the vocal cords will also lead to loss of speech. When you look up closely, phrenological claims such as "brain area X does Y" crumble, although certain brain areas are associated more with certain functions than others. Attaching a brain to a mechanical "body" to perform a function proves that a brain cannot affect the world and receives no sensory inputs without a body. The body is not just the hardware that runs some neural software, it determines how the brain works and provides it with its purpose. You just need both by order of evolution.

@vkehayas - "phrenological claims"? Phrenology infers characteristics from the shape of the skull, not the brain, and no normal modern person believes that. The brain would work pretty well if it had the right (and uninterrupted) conditions of nutrients, gaseous exchange, temperature, etc., but no one can come back from that to tell about it. And of course, sensory input would be gone, but that doesn't mean thinking would disappear. Insanity might ensue, but we don't know, we can't know. A quadriplegic has decreased sensory input as well, but can still think.

@anongoodnurse Do you mean that you agree with my arguments or that you missed their point? Because demanding absolute localization of cognitive functions in a one-to-one correspondence with specific brain areas is high-resolution phrenology and it's not supported by evidence. As for artificially re-creating the physiological environment that the rest of the body provides for the brain to sustain its function, you must be able to see that it re-inforces my argument, right? Lastly, does a quadriplegic's condition suggest to you that the body is not necessary for cognition? If so, how?

@vkehayas so you think a computer needs the internet to run programs just because it needs the internet to download them? As a pointed out a brain in a vat of jelly connected to nothing but wires can still learn, input is needed but a body is not the only form of input.

@anongoodnurse Unfortunately I do not have the time nor do I think this is the place to have such a discussion. If you are curious though, I encourage you to read primary research or at least something recent (last 40 years or so). On the topic of the dualism you appear to espouse, read on "embodied cognition", e.g. Damasio, Varela, Lakoff etc.

@John Imagine a computer that atrophies if it stays unplugged from power or disconnected from the internet and that can only grow if those conditions exist. Now imagine a computer that can have multiple power sources and ways to connect with other computers and grows --in a similar way to biological evolution-- according to the sources available and those that it "prefers". I encourage you to read about structural and functional plasticity during development and in adults. I do not doubt that if we try we will be able to sustain a healthy brain without the rest of the body. But why?

@vkehayas none of which shows cognition is not happening in the brain, it just shows that the brain needs certain conditions to operate, which well duh.  I am curious as to what you think is being argued because you don't seem to be giving any arguments against the brain being where cognition happens, just that the brain is not the only part of the body, which nobody is arguing.

We can monitor brain waves from people in comas and brain death. Even though their organs are fine and so are their heart and limbs, their brain scan looks like this:

Thank you. However, I would beg you to consider that this is only an evidence for brain having a critical role in cognition, not an almost exclusive one. I know that there is enough evidence for brain having a critical role in cognition, however my curiosity was mainly that how can we confine it to the brain alone. In other words, how can we be certain that cognition is not spread throughout the body.

To support such a claim, you need to be able to answer questions such as: "What led to coma/brain death?", "What is the result of the loss of brain function?", without invoking the rest of the body.


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Which horn configuration is more effective as a weapon?
For horned animals, there are two common configurations of cranial horns.

One long horn above the nose (Styracosaurus, Rhino).
Two long horns above the eyes or forehead (Triceratops, cattle, African Buffalo).

In many species, the cranial horns are used as a weapon: both for intra-specific combat (e.g. dueling over mate) and defense against predators.
My question is which configuration is more effective and lethal: 1 nose horn or 2 brow horns?
I suggest dividing the answer into two categories: Ceratopsid dinosaurs and extant mammals.

Why might that be that the vast majority on horned animals are two horned?

In dinosaurs, single-noseed-horned ceratopsids were abundant as well.

My question is about the present, not the past. Did you do any research about this yourself? What did you find out? On this site, failure to present some search result is a reason to down vote and close vote, so if you're done any, it would be beneficial to you to quote and link to it.

Also at play are other components of anatomy: stature, closeness to ground, skull strength, neck muscles, core/limb design/musculature... Not to mention environmental drivers for these adaptations: substrate texture, compaction, slope, etc. In the end, asking which is better isn't really a great biological question. Both evolved in response to ancestral morphological traits adapting to different environments/behaviors. I don't think the question needs to be closed, per se, but I think it's a low quality question as written. I hope the eventual answer includes mention of the issues I raise.

this is pure opinion, what is best is going to depend on the rest of the skull and the rest of the animals anatomy, how it can move and balance. then you have to consider lethal against what? different attacks work differently against different predators.

Note
Since a lot of people are upvoting this (and some downvoting of course), it's worth noting that it's not directly answering the OP's stated interests of dinosaurs etc. However, I think it's probably a more useful answer in general for people interested in horned animals.
Not intended to be the only answer on this question!
Answer
This doesn't fit neatly into your dinosaur vs mammal dichotomy, given the obvious differences in ecology and biomechanics, but I would suggest looking at horned beetles to think more about the effectiveness of horn weapons in different contexts. In some cases both configurations you describe (among others) are present in the same species and vary widely in the same genus.

One review paper here suggests that behavioral variation can account for the presence/absence of horns across species:

Thus, tunneling likely set the stage for the evolution of one-on-one fighting in tunneling taxa, such as Onthophagus, and the evolution of weaponry, such as horns, that is useful in one-on-one combat and in the blocking of narrow tunnels to prevent other males from accessing the female.6,26 Consistent with this scenario, horn possession is widespread and elaborate in tunneling scarabs, where it appears to have evolved independently several times, yet is virtually absent in any other group of non-tunneling scarabaeine beetles.31

One paper cited in that review presents phylogenetic comparative evidence for this view, in the following figure:

These suggest that the horn morph in question (triceratops-style) is useful in intraspecific sexual competition in a physically constrained context yielding single opponents (tunnels). This is somewhat similar to familiar examples in large mammals that do "single combat" mating competition. Direct confirmatory tests of this hypothesis were performed in separate work. There is some evidence in related beetles that this is particularly in response to an environmental stimulus of high beetle population density, and thus intensified sexual competition.
Thus, intraspecific sexual competition appears to be responsible for horn emergence in most cases. One classic study looked for ecological correlates of evolution of various horn configurations in a phylogenetic context, though the results seem ambiguous to me due to the quite small number of taxa. Nonetheless, the study highlighted a possible tradeoff between head horn presence and flying, and the presence of horns on the head in some ecological contexts. So, elaborate or large horns specialize the organism for fighting rather than for other activities.
One likely hypothesis is that mating competition is severe enough to drive an evolutionary arms race, leading to horn innovations that might yield advantages. Agent-based modeling approaches support this general theory, but no one seems to have directly tested this hypothesis with real beetles.


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What kind of spider is it and was this web built beforehand? (Surprise find)
I am surprise to find an insect caught at the end of what seems to be very long nearly invisible thread/web, most importantly where the insect is caught is actually a passage way where we enter the house so there seems to be no chance for this web to be there unless it was built in few hours!
Questions: What kind of spider could this be and could the web have been there all along or it was built instantly? Do these spiders build lots of long thread like webs in hope of capturing prey one day as I have never seen such web anywhere in my house. Will the spider roll up its prey or will eat it there? I want to know this because I am anticipating guests tonight so cant have it lingering there, unless it eats up the prey fast or takes it up to the ceiling.

P.S. I am going to let the spider do its business to see if its going to take the insect back up or will eat it there itself.

For ID questions like this, you should give as many details as you can: where in the world the picture was taken, what time of day, etc. and especially about how big the subjects are.

the picture was taken in Dubai, at around evening. I am not sure about the size because I didnt want to touch the subject. However surprisingly after 1 hour the spider and its prey was gone.

The pictures don't show the eyes, but from the shape of the cephalothorax, this is a jumping spider. Large ones are about 1 cm long, so unless that moth is huge, the size range fits. Here's a user-submitted picture from spiderid.com showing Platycryptus undatus feeding in a similar way:

Jumping spiders frequently attach a silk dragline to the ground before jumping. This functions as a safety line if they miss, but also allows them to change their position in midair which helps them to land on their feet even on surfaces that aren't parallel to the one they jumped off of.
So, probably the spider saw the moth resting on the wall or wherever, jumped on it and injected venom, the moth dropped from the wall and tried to escape, but the spider attached the dragline to it. Possibly the spider then retreated up the silk line to wait for the moth to die, and went down to feed once the silk line stopped moving, which is when you found it. The picture above came with a comment that the spider ate its prey in-place, so yours probably will not try to move the moth.

I believe the spider was around 1cm long . But after an hour both were gone. I thought it might have fell on the ground cause if you watch the video there was wind blowing from the window, I am not sure how resililent the silk is, but I couldnt locate it in the floor.

Thank you, +1. Fun to learn new things about my favorite kind of spider!


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Is ghrelin only secreted when the stomach is empty?
Several texts indicate that ghrelin is secreted when the stomach is empty. However, some(not all) texts also indicate that ghrelin is secreted when blood sugar levels are low. Is the second statement true? If so, how does it relate to the first statement?
Consider a hypothetical situation:A person drinks water at regular intervals such that his/her stomach is sufficiently full throughout the day.During this period he doesn’t eat and his blood sugar level is low. Would ghrelin be released at any point in such a situation(excluding the night)?


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The springlike behavior of titin problem
I am currently reading a textbook (Molecular Biology of the Cell, 6th ed), and this problem on p. 170 is driving me crazy. I read through the solution given in this book but I couldn’t understand it after all.
Here’s the question:
Titin, which has a molecular weight of about 3 × 106, is the largest polypeptide yet described. Titin molecules extend from muscle thick filaments to the Z disc; they are thought to act as springs to keep the thick filaments centered in the sarcomere. Titin is composed of a large number of repeated immunoglobulin (Ig) sequences of 89 amino acids, each of which is folded into a domain about 4 nm in length (Figure Q3–2A). You suspect that the springlike behavior of titin is caused by the sequential unfolding (and refolding) of individual Ig domains. You test this hypothesis using the atomic force microscope, which allows you to pick up one end of a protein molecule and pull with an accurately measured force. For a fragment of titin containing seven repeats of the Ig domain, this experiment gives the sawtooth force-versus-extension curve shown in Figure Q3–2B. If the experiment is repeated in a solution of 8 M urea (a protein denaturant), the peaks disappear and the measured extension becomes much longer for a given force. If the experiment is repeated after the protein has been cross-linked by treatment with glutaraldehyde, once again the peaks disappear but the extension becomes much smaller for a given force.

A. Are the data consistent with your hypothesis that titin’s springlike behavior is due to the sequential unfolding of individual Ig domains? Explain your reasoning.
B. Is the extension for each putative domain-unfolding event the magnitude you would expect? (In an extended polypeptide chain, amino acids are spaced at intervals of 0.34 nm.)
C. Why is each successive peak in Figure Q3–2B a little higher than the one before?
D. Why does the force collapse so abruptly after each peak?
The solution:
A. These data are consistent with the hypothesis that the springlike behavior of titin is due to the sequential unfolding of Ig domains. First, the fragment contained seven Ig domains and there are seven peaks in the force-versus-extension curve. In addition, the peaks themselves are what you might expect for sequential unfolding. Second, in the presence of a protein denaturant, conditions under which the domains will already be unfolded, the peaks disappear and the extension per unit force increases. Third, when the domains are cross-linked, and therefore unable to unfold, the peaks disappear and extension per unit force decreases.
B. The spacing between peaks, about 25 nm, is almost exactly what you would calculate for the sequential unfolding of Ig domains. The folded domain occupies 4 nm, but when unfolded, its 89 amino acids would stretch to about 30 nm (89 × 0.34 nm), a change of 26 nm.
C. The existence of separate, discrete peaks means that each domain unfolds when a characteristic force is applied, implying that each domain has a defined stability. The collection of domains unfolds in order from least stable to most stable. Thus, it takes a little more force each time to unfold the next domain.
D. The sudden collapse of the force at each unfolding event reflects an important principle of protein unfolding; namely, its cooperativity. Proteins tend to unfold in an all-or-none fashion (see Problem 3–35). A small number of hydrogen bonds are crucial for holding the folded domain together (Figure 3–39). The breaking of these bonds triggers cooperative unfolding.
If so, I think the graph should look somewhat similar to this:

or this:

*I didn’t scale the graph because I don’t know the exact figure.
Since the protein unfolds in an all-or-none fashion, it won’t extend until it is unfolded, but it will extend gradually as it unfolds.
As it takes a little more force each time to unfold the next domain, the constant portion of the graph should be lengthened as the domains progressively unfold.
In both graphs, the extended lengths are always the same, but in graph 2 the domains get harder and harder to unfold so they require extra input of energy each time they unfold. (Thus the slope of the diagonal portions of the graph needs to be less steepened.)
I don’t know which one is correct, so I drew both.
The question is, why is my answer different from that of the textbook? Is there something wrong with my reasoning?
Any idea or answer is appreciated!

When an Ig domain unfolds, its length increases, so the force required to stretch the whole protein to a given length will decrease. Your diagrams don't account for this decrease in force.
You can think of the domains like wire coiled into the shape of a stereotypical spring when they are folded, and a straight line when they are unfolded. Stretching the coiled spring to the length of the straight wire will take a lot of force. Obviously no force is needed to keep the straight wire at its natural length. (This isn't true of unfolded proteins, but the entropic force is small compared to the elastic resistance from the folded domains)


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What proportion of lung compliance is attributable to alveolar surface tension?
I am reading Guyton and Hall, chapter 38, Pulmonary Ventilation. It states that the two main factors influencing lung compliance are 1) tissue elasticity 2) surface tension elastic force. An experiment is used to illustrate that one surface tension requires far more pressure to overcome during respiration than tissue elasticity, see diagram.
The text then states that because the pressure difference in the normal lung is about three times greater than the saline-filled lung (which has no surface tension effect, only tissue effects) that one can say that lung elasticity is only about one third tissue elasticity and two thirds due to surface tension elastic force.
My question is that given lung compliance is the reciprocal of lung elasticity does this mean that lung compliance is more due to tissue elasticity?
"Lung compliance is the volume change that could be achieved in the lungs per unit pressure change. [Lung e]lastance, also known as the elastic resistance is the reciprocal of compliance, i.e. the pressure change that is required to elicit a unit volume change. This is a measure of the resistance of a system to expand (Kahathudwa 2022)."
References:
1:
[2] https://owlcation.com/stem/Lung-Compliance-and-Elastance
[3] Guyton and Hall Medial Physiology, Chapter 38.
[4] Stat Pearls, Pulmonary Compliance, https://www.ncbi.nlm.nih.gov/books/NBK538324/


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Does decellularization with sodium lauryl sulfate break down enzymes?
I am currently looking into decellularization with sodium lauryl sulfate since it is effective and cheap. My goal is to break down the cells of a plant leaf and release the chloroplasts to be viewed under a microscope(I realize you can do this without decellularization but I'm still curious). My question is, will sodium lauryl sulfate break down the cell membrane and cause no further damage to the organelles or enzymes? If not, what chemicals can break the cell membrane without causing any more damage to the organelles or enzymes?

Welcome to the site. Please take a [tour] and visit the [help] for more information about this Stack and what we do here. In addition please note the homework policy, which generally asks that the person asking the question demonstrates what they know about their question. So... what do you know about SDS/SLS and its chemistry?


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Size ratio of Drosophila bifurca gametes and implication for the definition of sex
I recently learned that males of Drosophila bifurca species have gigantic sperm cells, 5.8 cm long and they only produce few hundred such cells during its lifetime. This made me wonder if the male gametes are larger than the female gametes in this species? If so, it would mean we are naming males and females incorrectly in that species, as according to definition, males and  females are determined by gametes size [1]. However I cannot find any information about exact size (length of sperm is not enough) or weight of their gametes nor even a picture where both are present next to each other.

Wikipedia definition :P https://en.wikipedia.org/wiki/Anisogamy https://en.wikipedia.org/wiki/Sex

I've honestly never heard of sex solely being defined by the relative size of the gametes. That may be a rule of thumb, but size alone doesn't affect anything downstream, like sexual development pathways. That is determined mainly genetically, and in some species environmental factors such as temperature can play a role.

@David I added link to https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5031617/

@MattDMo Yes, sex can be determined genetically or by environmental factors... but then how do you decide which one we would name "male" and which one "female"?

I think there is some confusion in the comments. OP is not talking about sex determination, but rather the very meaning of male and female. The meaning of male and female is typically made in consideration of gamete size, where the female sex produces larger gametes.

@David What else would define the sexes across taxa? OP includes a reference to a discussion of the development of sexual differentiation from isogamy, it seems pretty clear.

@David I could dig a bit but I don't know where it originates. My own training in biology came substantially after 1972 :)

Thanks @BryanKrause . I've posted an answer now, and this encompasses the points made in my comments, so I have now deleted the latter. As I mention in a footnote, I would still be interested in information about the origin of the gamete-size definition of sex.

I've edited your title to indicate its broader motivation. I hope this may bring it to the attention of more biologists with knowledge of the history of the definition at issue. You are, of course, free to revert if you are unhappy with the edit.

Relative size of gametes
The relative sizes of the sperm and eggs of D. bifurca can be seen in the scanning electron micrograph below, taken from a 2006 Nature paper by Bjork and Pitnick.

The left-hand frame (a) shows a single, 6-cm D. bifurca spermatozoon dissected from the seminal vesicle, where sperm are individually rolled into compact balls. In the right-hand frame (b) six of these have been reduced to the same scale as a D. bifurca ovum and placed alongside it.
It is clear from this that the ovum is much larger than the sperm. I do not think the absolute sizes of sperm and ovum are the point at issue here, but the poster or interested reader can calculate the volume of the ovum from the micrograph above, and that of the sperm from highly detailed electron micrographs in Fig. 6 of a 2008 publication of Dallai et al.. The latter appear to have a cross-section diameter of approx. 0.7–1.0 μm. (Egg volumes for some other Drosophila species can be found here.)
Even if…
Although I think that the section above answers the question, there is a relevant aspect of fertilization in D. bifurca that should be mentioned. This is that, in contrast to Drosophila species with smaller sperm, only a portion of the sperm of D. bifurca actually enters the egg. This is shown in the image below in which only 1.6 mm of the 58 mm long sperm (about 3%) penetrates the egg (only part of which is shown).

(Visualization of sperm in fertilized eggs of D. bifurca. From Karry and Pitnek (1996) Nature 379, 405–6)
Thus, in principle, a giant sperm with a volume of perhaps twice that of the egg would still be able to penetrate and fertilize the latter. The implications of this are considered briefly below.
Implications for definition of male and female gametes
What would the implications be for a Drosophila species in which the volume of the ejaculated sperm exceeded that of the egg, but by an amount that still allowed penetration of a portion containing the nucleus, which could then fuse with the egg nucleus?

Would it mean — as stated by the poster — that “we are naming males and females incorrectly”?

I assume that, like D. bifurca, individuals of this hypothetical species display similar marked sexual characteristics to other species of Drosophila, genetically, physically and behaviourally. In this case, giving the assignation female to what in other species are called sperm (and by implication giving this designation to the individuals from which they originated) seems patently absurd.

I would say that it is the definition that would need changing, not the sex.

Is the definition absolute?
As a molecular scientist with a chemical background who last studied organismal biology at the age of about 14, I was surprised at this definition. The paper cited in the question (published in 2016) makes the statement

“Even when there are no separate male and female sexes as such (i.e.
simultaneous hermaphrodites), there is dimorphism at the gamete level,
where clearly diverged male and female gametes are produced—male
gametes being by definition the smaller ones”

It may be thought that the implication is that individuals that produce male gametes are male, and those that produce female gametes are female, but this is not always the case (e.g. simultaneous hermaphrodites).
Judging from the Wikipedia article on anisogamy (the phenomenon of different sized gametes) and popular scientific websites, this seems to be generally accepted by biologists, but I have had difficulty finding when and by whom it was proposed, and what justification was given for the definition. The paper mentioned points back to one by Parker et al. in 1972 but that paper does not even state this explicitly — it is merely implicit in mathematical modelling of the evolution of gamete dimorphism.
I can only suppose that the original definition was based on a need to define male and female gametes in circumstances such as simultaneous hermaphrodites. The definition adopted was consistent with the situation observed in clearly sexually differentiated situations where the male sperm enter the larger female ovum, and so must have seemed a neat solution. However, as we have seen, in Drosophila with giant sperm, only a portion enters the egg, and this is sufficient because only the nuclei of the gametes need to fuse and form a zygote. Biology is not one of the exact sciences, and such a case would not be the first time a definition needed to be tweaked or to admit exceptions.

Footnotes
I thank Professor S Pitnek for directing me to the papers with scanning electron micrographs of the sperm and egg of D. bifurca. If anyone can cast light on the origin of the size-based definition of male and female gametes I will edit this answer to accommodate the information.


text:
How deep under water can humans open their naked eyes without damaging them?
Humans can tolerate a maximum pressure of 100atm, but it becomes uncomfortable above 30 atms. Deep divers usually wear protective equipment like goggles among other things and our eyes seem to be more fragile than the rest of our body.
So, without using goggles how deep can a human open their eyes under water before suffering from an injury?
The injury, I believe, would be the eye getting crushed by external pressure.

I could be wrong but I can imagine that it doesn't matter much whether you have your eyes open or closed in terms of protecting your eyes against pressure, so it's merely a question of how deep can you go without wearing goggles/mask.

A mask doesn't protect a scuba diver from water pressure, the surface air in a mask will shrink to a 1mm bubble at 300m, and scuba divers often fill their mask with water at any depth to get rid of condensation, to adjust the straps, to fix the red lines and have a scratch. So mask or no mask it doesn't matte. A mask doesnt provide any pressure protection whatsoever. https://youtu.be/PuVXxj70s1w?t=38

@Ivo My eyelids do nothing!

I wonder: What makes you think the heart or ears are not crushed by the pressure? Also "naked eyes": What effect do you think goggles have? Obviously the pressure is the same.

@U.Windl Yes, the pressure would also affect the heart or ears, but my question was directed at the eyes in this case. By goggles, I was referring to protective equipment used by divers. Although now I have realised wearing goggles/masks will not have any effect.

Crushing damage from pressure occurs due to pressure differences. Imagine you have a rigid container. If you have equal gas pressure inside and outside, the pressure acts on just the walls and the container will survive unless the pressure is high enough to heat/melt the walls to failure. However, if you have high pressure outside and low pressure inside, you can expect the vessel to at some point violently collapse due to the pressure difference.
When diving with a mask, it's important to equalize the pressure inside and outside the mask. E.g. from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4943308/

Diving can affect the IOP [intraocular pressure] in a number of ways; firstly from the change in the internal mask air pressure at different underwater depths, secondly from the inhaling or exhaling from the nose, and thirdly through the diving mask itself. The first and second factors can be controlled by the diver by exhaling from the nose during descent, also known as equalizing the mask pressure. Senn et al. [5] found that diving mask pressure spikes were less common in experienced divers compared to beginners. Failing to equalize the diving mask pressure can lead to ocular barotrauma, which ranges from lid edema, ecchymosis and subconjunctival hemorrhage to more serious injuries such as hyphema and subperiosteal orbital hemorrhage [6, 7]. The diving mask itself may also affect the IOP. Swimming goggles are known to increase the IOP, with larger-frame goggles having less effect than smaller-frame ones [8,9,10].

Or from https://www.ncbi.nlm.nih.gov/books/NBK545224/

Mask squeeze is a type of facial barotrauma injury that occurs most commonly while self-contained underwater breathing apparatus (SCUBA) diving or freediving. This condition occurs when divers fail to equalize pressure in the face mask to the surrounding water pressure as they descend. The result is a negative pressure (relative to the surrounding water pressure). The difference in pressure inside and outside the mask can lead to injury of blood vessels and tissue of the eyes and tissue covered by the mask, including forehead, nasal areas, and periorbital regions. The main risk factor for a mask squeeze is the inexperience of the diver. Masks with high internal volume or the use of snorkeling masks or swim masks that do not cover the nose can also increase the risk of this type of injury.

Or, in simpler phrasing, if you have low pressure inside a mask and high pressure inside the rest of the body, the pressure difference is going to push/suck the eyes outward and crush the blood vessels or damage the eye itself. You want to have the same pressure pushing on the eyes from the outside and inside. It's really no different if you 1) have high pressure outside the mask and 'normal' pressure inside the mask, or 2) have low pressure (vacuum) inside the mask and 'normal' pressure outside: both situations have a pressure difference, and it's the difference that does the damage.
So, to answer your title question, a mask is more likely to increase pressure risks to the eyes rather than to decrease it.

I remember one of the record seeking deep divers (those that must use their own custom-made equipment) say "there is essentially no limit to the pressure the human body can sustain". I was not able to find that statement again and it may not be entirely correct (especially the gases solved in the blood can be damaging) but the body can certainly sustain much more pressure than one would perhaps naively think. When in hydrostatic equilibrium, pressure as such is mostly unnoticeable.

@Peter-ReinstateMonica - A sphere is the shape best suited to resisting external pressure; a cylindrical object is next. If there are depths to which cylindrical objects cannot descend (submarines) without imploding, I would imagine there are depths to which humans cannot descend. It's not about "hydrostatic equilibrium" or gasses; it's about the weight of water the further down you go.

@anongoodnurse The difference between a submarine and a diving human is the difference -- in pressure: There is no pressure difference between the "inside" and the outside in the case of the diving human, so there are no forces (or, if you want, there are huge forces, but they cancel each other out). By contrast, the submarine (typically) retains its internal pressure of one atmosphere when diving and thus has to withstand a huge pressure difference resulting in huge forces that try to compress it.

@anongoodnurse To elaborate: Because the body is mostly water and solids it is largely incompressible. It's essentially like submerging a water balloon with a few bones in it: No forces whatsoever. The exception are the gas-filled lungs and the changed solubility of gases in fluids (blood) under these pressures. The lungs need to be filled with equally pressurized oxygen mixtures (I'm sure the bottles with the required mix and pressure are an example of the custom-fitted equipment). High partial oxygen pressures are toxic, nitrogen is a no-no etc.

@Peter-ReinstateMonica - That all makes sense in a way (and I see that the submarine comparison was not well thought out.) But I can't imagine being able to expand the chest against 500 atmospheres. And you're right about dissolved gasses (I just did a bit of quick reading), but I'm stuck at being unable to breathe.

@anongoodnurse, if you're filling your chest with gasses that are at the same pressure as the water outside, there's no differential to fight.

@Peter-ReinstateMonica I have always wondered about pressures in the body that are not able to or which have impediments towards normalizing the pressure differential.  For instance, it is possible for gasses to form along the entire digestive tract, how would it be possible to equalize pressure without essentially "swallowing" air at a higher pressure?  It seems like you couldn't (e.g.) burp to get rid of such gasses if the air pressure outside was larger than inside.

And if the pressures equalize by compression, then it seems like there would be an upper limit due to the fact that you now have extra pressure compressing an internal space in your body through your body.

@Michael Gases in cavities within the body are really only a problem during decompression. As you increase pressure, any existing gas bubbles will get smaller. Bubbles getting smaller don't do any damage. However, if you have a bubble under pressure (dissolved or not) and then decrease the pressure, the bubble gets bigger, and if it gets bigger than the cavity holding it, you're going to have problems. The main problem is with dissolved gases coming out of solution in the bloodstream and occluding vessels, because the surface tension at the blood-gas interface is stronger than blood pressure.

@anongoodnurse One cannot even breathe under 2 feet of water under one's own power because the pressure is already to high (here is a page that has a good description). When scuba diving, the air in the bottle is pressurized and "forced" into the lung, equaling out the pressure. That is very much like we are breathing at sea level, under quite some pressure: The pressurized air around us enables us to breathe at all.

@anongoodnurse: A SCUBA regulator is a key part of the setup: its input is high-pressure air from the tank, its output is air at about the same pressure as the water, so you can breathe from it without needing to fight the water pressure or having your lungs over-pressurized and pop.  https://en.wikipedia.org/wiki/Diving_regulator - they have some mechanical valves that are controlled by ambient pressure (of the water).

@PeterCordes Ah, I wondered about that, thanks.

@Peter-ReinstateMonica - I understand now and believe you. Thanks for sticking it out with me. TIL!

@PeterCordes - Hard to wrap my head around such a sophisticated system, but I understand and thank you, too.

Goggles do not, cannot, protect eyes from pressure. The pressure on both sides of goggles should be nominally the same. In fact, divers tend to use a mask, which communicates with the nose, to be able to equalise the internal pressure with ambient easily, rather than goggles which can damage the eyes if a descent is made without awkardly adding air by exhaling bubbles while lifting the lower edge of the goggles. The only thing that can isolate you from pressure at depth is a rigid suit, or a diving bell.
So why do people wear goggles/mask underwater?
The main reason professionals wear them is to keep a layer of air in front of the eyes, so that the eye lens is working between the correct refractive indexes and giving you normal vision. Replace that air with water and everything becomes very blurred. Basically the front face of the eye lens stops bending light, so you become extremely long-sighted.
The main reason amateurs wear them is to avoid the yuk factor of opening eyes under water, or irritation from biocides in the swimming pool.
There are multiple things that limit the depths divers can reach, but none involve the eyes.
Oxygen toxicity and nitrogen narcosis limit compressed air or nitrox sport dives to a few 10s of metres. To go deeper one needs extensive decompression time and/or expensive helium, and deeper still an addition of hydrogen. Regular commercial dives rarely exceed 300 m, with only the military accessing anything approaching 500 m. Studies (usually in pressure chambers on land) have pushed lower, but seem to run out of human tolerance for the effect of high pressure gases on the central nervous system in the 650 to 700 m range.
I did a short diving course, and the exam started with them throwing all the gear into the pool, mask included. The idea is that you need to be able to recover from an accident where everything is knocked off your face, and then some. So, open your eyes, swim to the bottom, locate blurry tank and take a breath, grab your blurry weight belt, locate blurry mask and put it on, breathe air into mask so now you can see properly, and it gets easier from there.

So the air inside the googles / mask is effectively another lens element between the eyes and the water. Importantly the rear of the air is shaped with a curve that conforms to the eye, and the front of the air is shaped with a flat or near-flat surface that conforms to the plastic surface.

@bdsl The air inside the mask is the dielectric constant that the eye has evolved to work with. Well, approximately at least. I'd imagine the refractive index of the gas increases slightly with pressure, but not to the extent that increases by replacing it with water.

@bdsl Yup, mask/goggles are basically corrective eyewear that since everyone needs the same prescription for and thus are stock rather than from an optometrist.

Currently the record for the deepest dive wearing scuba equipment is 332.35m. The descent took only 15 minutes while the ascent lasted 13 hours 35 minutes.
Liquids do not compress, so the sinuses, inner ear, lungs and circulation are in far more danger from pressure than the eyeballs.
The main danger is not the pressure at depth, it is the readjustment to the expanding gases as the diver rises, decompression sickness, which rarely affects the eyes.

This doesn't answer the question at all.

The question explicitly states "without using goggles". Goggles/masks are included in scuba equipment.

Yes, it does answer the question. Face and mask of the diver could never withstand such a pressure difference, meaning that the diver needed to equalize the pressure, which is normally done by taking of the mask and blowing (high-pressure) air inside. Descending so quickly, there is a chance that you can't get the mask off your face if you wait too long, meaning that pressure would build up until implosion, which would pose an enormous health risk. For this reason, such records are generally done without wearing a mask, while descending. The answer is that eyes are not the bottleneck.

@Ivo He said how deep and why, I said 325m is still ok, no evidence beyond that and some reasons.

@GoalaSestant that's with scuba equipment

@Mast There is no evidence beyond 325m but that's a good start for a general idea. Swimmers use goggles, goggles can't equalize pressure, divers use masks where they equalize the water pressure, it's easy to take the mask off at any depth. Opening the eyes underwater at 325 meters is fine.

@Ivo did you know that scuba equipment doesn't protect the eyes from water and water pressure, and scuba divers regularly take off the mask underwater and fill it with water to get rid of condensation and other reasons? https://youtu.be/PuVXxj70s1w?t=38

@GoalaSestant I'm guessing a lot of people are not aware, which is probably why you should amend your answer. I don't have a great understanding of what scuba gear protects, or when that protection is removed.

@GoalaSestant I didn't know. Thanks for telling me

The answer is incomplete, because at a depth of 100m the partial pressure of oxygen and nitrogen will probably kill your nerves (specifically the brain) (or at least make them inoperative). So there are special gas mixtures used then. For normal air the nitrogen-induced limit is around 56m.


text:
What is this fungus in my plant growth medium?
I am growing S. lycopersicum on 1x Gamborgs medium and have been getting some fungal like contamination. The media contains 0.2% sucrose and Bacto-Agar. Plants are grown at a 21 c - 20 c day, night cycle. The contamination is characterised by squiggly string like structures that penetrate the agar. Structures vary in size but are usually 1-3 millimetres.

EDIT:
Under Compound microscope:
100x

200x

400x

any chance you could pick a few out and get pictures on a slide under a compound microscope?

And an overall photo of the fungal colonies if you can get them. Also: this might be some use. They list several genera with spiral hyphae.

I will upload the compound now, it's not very clear as the structures are buried in the agar.

I have tried putting it under a slide but the stucture does not stay intact

Interesting - I don't see any cellular structures, but, as you say, this might be because of integrity and clarity issues. Could it be the track of something like a nematode or a protozoan, as it looks like a burrow?

Burrow like a leaf miner caterpillar might make inside a leaf that is. Though the regularity of the shape makes a biological structure more likely. Could you get a sample from each end and see what's there? An inverted microscope might be able to give you some depth if you are looking through the agar, but optical clarity will be a problem with the agar. Another thing to check would be to see if you can get it to replicate - take a sample onto a fresh plate (no plant) and see if it multiplies/grows.


text:
Absorption bands of chlorophyll
I am currently reading this article, which discusses the functional impact of the $Q_x$ and $Q_y$ absorption bands of chlorophyll in photosynthesis. However, the article didn't say where on the spectrum these bands exactly are. It did, however, say that the $Q_x$ band is also known as the $S_2$ band, and the $Q_y$ band as the $S_1$ band. I tried to resolve my question with some Googling, and found the following two pictures on the Internet. The problem is that these pictures seem to imply opposite things: one is claiming that the $Q_x$ band is the blue/violet part of the absorption spectrum while the $Q_y$ band is the red part, while the other claims that $Q_x$ and $Q_y$ are both red and practically superimposed on each other. So which one of these graphics can I trust? And can you point me to any articles that explain the $Q_x$ and $Q_y$ bands definitively?

Did you see this para in the article: "Historically, two different assignments of the spectra of Chl-a have
been proposed: the "traditional" 1960’s assignment identifies the
higher-energy component as the Q x origin 10,13–16
, while the "modern"
1980’s assignment selects the lower-energy one, see Fig. 2"

I don't pretend to understand the physics or chemistry of it, but I think you'll find that the Qx and Qy are vibrational states, sometimes referred to as S1 and S2, not absorption bands. Are you asking about the absorption spectra of chlorophyll or the transitional states?

@bob1: yes, but I thought that the article gave the bands in terms of $\Delta v$, a parameter in Magnetic Circular Dichroism measurements, which doesn't directly correspond to a given wavelength (I think). Am I wrong about that?

Mu might be wavenumber rather than a spectral measurement.


text:
What lysis buffer recipe is good for just breaking the cell membrane?
I am interested in the decellularization of plant leaves(more specifically maple) and thus need a lysis buffer. I want the buffer to only break the cell wall and cell membrane and I want to observe the proteins in the cytoplasm so the buffer can't be too strong as to deactivate the proteins/enzymes in the cytoplasm(I don't care about the nucleus). I looked at RIPA, SDS, and NP-40 but they are all too strong and can damage the proteins. Is it possible to only use salt in a buffer solution without any detergent and if not, could you please recommend me a lysis buffer solution? For more clarity, I am mostly interested in looking at hexokinase. Thank you for your time.

Look for lysis buffer kits labeled for creating nuclear extracts. There are generally two buffers: one to lyse the cell membrane, after which the lysate is spun down and washed, then a second buffer to lyse the nuclear membrane. I don't have time at the moment, but I'll try to find a reference for you later.

I just realized that you're talking about plant samples, where you also need to lyse the cell wall. Have you considered mechanical lysis, either with a mortar and pestle or sonication?

If I were you I would look into dounce homogenizers, along with the use of a cellulase to break down the cell wall.

Thank you for your answer, I have considered mechanical lysis but I am working with small samples so it isn't as efficient as chemical lysis. Mechanical lysis can also create localized heating which can denature some proteins so if possible I would use chemical lysis over mechanical. Using a cellulose is a good idea but I still need to break the cell membrane with chemical lysis

Also, can alcohol also break the cell wall like cellulase?

Centrifuge. Use a diluted salt solution and centrifuge the sample to separate the cell wall.


text:
Can the UGA codon be used as a drop-in replacement when adapting genes for Paramecium?
Question
It is well established that Paramecium translate UAG and UAA mRNA codons to amino acid, although they are STOP codons in most other eukaryotes. (https://www.nature.com/articles/314188a0)
Suppose I wish to express a particular bacterial gene in Paramecium by translation of its mRNA in a similar fashion to the SARS-CoV-2 (COVID-19) vaccines. The gene is AlkB from Alcanivorax borkumensis, which encodes foralkane hydroxylase (https://www.ncbi.nlm.nih.gov/nuccore/AB110225).
The coding DNA sequence of this gene ends with TAA (UAA in mRNA). As explained above, this won't be translated correctly by Paramecium. Could I simply replace the DNA TAA/mRNA UAA  with DNA TGA / RNA UGA in order to get it translated to the same protein in Paramecium?
Evidence of Research
This is only some of the research I have done for this question. More can be provided, if required.
Search on this site for previous similar questions https://biology.stackexchange.com/search?*q=can+i+switch+codons+with+their+equivalents yielded nothing
Paper  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5409834/
Not useful because it only states that switching mRNAs that mean the same thing may make translation take longer due to rare tRNAs. The only STOP tRNA in Paramecium has the anti codon ACU, as proved above.
Paper
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3549826/
Not useful because it's about bacteria.

Welcome to SE Biology. I have edited your question to improve the likelihood of its receiving attention and a positive response. This consisted of removing much inessential and repetitive material, and the over "loud" appearance through abnormally large text in headings. I also replaced the opening statement that "It is commonly known". Your view of what biological facts are known to this audience is irrelevant to the question, and off by a mile, in a way that antagonizes people who do not know. Likewise, we don't need to be told to click on links to find something out. But I'll answer it.

Hi @David! Thank you so much for your lovely edits & answer, it made the question a lot better! I didn't mean to really offend anyone, thank you for correcting the language used. :)

Preamble
The choice of the organism and gene for expression is not explained, although I gather the bacterium is able to degrade oil components using this enzyme. However one wonders why anyone should wish to express the enzyme in Paramecium, which to my knowledge has not been used to express foreign nucleic acid sequences. The mode of delivery of foreign genes or mRNAs is an important consideration in their expression, but I shall ignore this in my answer. However as Covid vaccines are invoked in the question, a study of papers reviewing the structural features of mRNAs that facilitated their expression (e.g. this one) is advised.
Answer

In principle, replacing a UAA stop codon by a UGA stop codon should still allow termination of translation, especially in an environment in which UAA is the only stop codon. The only possible problem I can see is that of possible readthough, which can occur in certain sequence environments. However if the protein is terminated properly in the bacterium, there seems no reason to expect a disfavoured environment in Paramecium.

As we are considering the expression of a bacterial mRNA in a eukaryotic environment, the differences in bacterial and eukaryotic translational initiation (see any decent biochemistry text or search this site) need to be considered as well as termination. In brief, eukaryotic initiation occurs at a capped 5′-end, with the ribosomes then progressing to what is generally (but not always) the first AUG. An mRNA containing the bacterial coding sequence would have to be synthesized that facilitates this. In addition, polyadenylation of the 3′-end is required to ensure a stable mRNA. A close examination of the features of Paramecium mRNA sequences would be prudent before undertaking such a project.

Thank you - that answer is so great and I understand now  Unfortunately I cannot up-vote yet, but it is a great answer well-written well answer well worthy of one.

I'll definitely do the research you suggested, looks like a great rabbit hole to go down...


text:
How to theoretically calculate amount of product in first-order reaction?
I was wondering if it was possible to calculate the amount of product theoretically produced from in vivo (human) values to determine if that's the only enzyme causing the increase in amount of product. The rate of the reaction is dependent on enzyme concentration, and assumes that enzyme $K_m << [product]$ (in rats at least).
From the papers I have read, others have calculated the theoretical concentration (in rats) by:
$[product] = (k_{cat}/K_m) * [substrate] * [enzyme]$
However, as far as I remember $K_m$ is dependent on multiple environmental factors and $K_{cat}$ can change as well.
Thus, I'm wondering how I could theoretically calculate it.
Post-edit:
My questions are more this:

Can I use the $K_m$ and $K_{cat}$ I found in papers for the reaction (also found in humans), given that they differ greatly between papers.
Is the equation given above correct for a first-order reaction?
Any papers or books I can read to learn more about this?
Any ideas to calculate this?

I suggest googling the issue a bit, this paper that I found quickly looks like it addresses some of your concerns directly (notably accuracy of K parameter estimates). Also it would help to link some of the resources you seem to have found.

You need to set out your problem — or an example — with actual values, and what you want to calculate. Without this I doubt whether anyone can help you.

The answer to question 2, I think, is an emphatic yes, provided that the substrate conc is way below Km (the Michaelis-Menten equation then describes a first-order reaction).  Two great sources are Fersht Structure and Mechanism in Protein Science and  Frost and Pearson Kinetics and Mechanism


text:
Is there a term for a sequence of genomes for a family?
Suppose that I am following how a "familial" genome changes throughout generations. That is, I have the genome of a grandmother, father, and daughter, and my objective is to see how the genome of each generation changes. Is there a better word for "familial genome," which defines the sequence of genomes through genetically related individuals?

When you write "sequence" in the titles do you mean "sequence" in terms of DNA sequencing, or are you using in a more general way to mean successive arrangement of grandparent/parent/child?

@BryanKrause Great question. I meant the latter. Thanks for clarifying :)

Update
Based on conversation in the comments below, it seems that the the OP is interested in how reference genomes can be used to represent the background genome on which variants can be used to represent the specific genomes of individual people.
Original answer
May be misunderstanding, but I am not sure that the concept that you are talking about actually exists. Recombination in each generation will break up contiguous chromosomal sequences into shorter regions that are passed down each generation. Furthermore, such a familial genome has an artificial bound, as ultimately all humans are related in a single pedigree due to the likely single origin of humankind.
Some related concepts are:

pedigrees
trios (parents and child genomes sequenced, usually to track where a child's genetic disease comes from)
quads (parents and two child genomes sequenced, usually where one child is affected by some genetic disease- no convenient link but similar to trios)

The closest thing to what you are talking about is probably the haplotypes shared by all family members. Haplotypes are the regions of sequence that can be shared by families that are not broken by recombination. You could speak of the set of common haplotypes between some set of people (in a family or just in a population).
However, haplotypes will necessarily get chewed up by recombination over time, so they're more of a heuristic for talking about the set of shared genotypes in a group of people (who are after all still related in some big pedigree), not something that's specific to lineal descent of families such as you suggest.

Thank you for your answer. This makes more sense. Suppose that I have genome sequences of different people in NYC (who are likely not family members). Would it be fair to treat their collection of genomes as a single genome that varies through time? I know this is odd, but just curious!

@RonSnow I don't know how you would make it "vary through time", but one standard practice for representing human genomes is to have a "reference" genome with some set of sequences for each chromosome, and then to represent individual peoples' genomes only by how they vary from that reference. This simplifies genome analysis somewhat, though it has its own set of issues. It seems like it might be similar to what you mean?

I think that is the closest thing to what I mean - you're correct. Thank you for your help! :)

@RonSnow updated answer to reflect this, no problem.

Perfect, thank you so much!


text:
Why would GREML in GCTA treat SNP effects as random effects?
I've read many papers, but none of them gave clear answer to my question.
For example,
https://www.nature.com/articles/s41576-019-0137-z#Sec5

The univariate GREML approach can model multiple random effects and
hence estimate multiple genetic variances using multiple GRMs, each
built with SNPs selected on different annotations.

https://www.nature.com/articles/ng.608

The effects of the SNPs are treated statistically as random, and the
variance explained by all the SNPs together is estimated.

I've also read that random effect refers to random grouping (site) effects. Why should SNP be considered groups?

Linear mixed models are used in genetic association studies because if you try and fit SNP effects using a straight forward fixed effects linear model and ordinary least squares, there is a tendency to overfit the $p$ (where $p$ is a large number of SNP densely located SNPS in some kind of LD) model parameters, as SNPs are often in strong linkage disequilibrium with one another (i.e. the SNPs effects are non-independent). Instead, if you treat SNP effects as random effects, you can restrict the SNP effect parameter values to a joint 'variance parameter' which is estimated from the data. In other words, we want to estimate a single 'shared' variance parameter value rather than many parameters for all $p$ SNPs to avoid overfitting the model.

Thanks for your answer. Do you know if there is a model that can take continuous variables as random effect? https://stats.stackexchange.com/questions/605703/is-there-any-regression-allowing-correlated-values-other-than-lmm


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Explaining "paraphyly" for the layperson?
I was a molecular biology major a while ago, but I never think I really understood cladistics TBH. Now reading about paraphyly, it shows this:

In this phylogenetic tree [second image], the green group is paraphyletic; it is composed of a common ancestor (the lowest green vertical stem) and some of its descendants, but it excludes the blue group (a monophyletic group) which diverged from the green group.

Looking at the "simiiformes", I can understand why you would call that "monophyly", because everything is connected to a common ancestor. But why not just make the blue area a full blue triangle to make the prosimii and simiiformes one triangle/group? In the end, we all share the same ancestor, so I don't see why they are disconnected.
TBH I'm not sure how to read this at all, and am not following the Wiki description. Can you explain how the 3 terms work for a child or layperson with a better concrete example?
We are all composed of atoms, so we are all made of matter. Matter is made of particles, so we are all made of particles. But light is a particle and we are not made of light, even though in some way "we share the same common ancestor" of the quantum field. But light is still called a particle, so the triangle is the group of all particles. I'm not sure I'm getting on the right track.

A paraphyletic group is a monophyletic group from which one or more subsidiary clades (monophyletic groups) are excluded to form a separate group.

Why would they do that?

I don't think any child or layman will ask for an explanation of "paraphyly" ;)

"We call all of these 'trees', but actually they are a wide range of unrelated plants."

@KevinKostlan - your layman's explanation is more charitable than mine, which is "Taxonomy is a giant sham, genus/species etc is a description that, as we dive into the genetics, is harder and harder to force into reality. So we keep screwing with the data to try and make it fit, because "new species" is a concept the public think is cool, whereas "genetically distinct group" is not. Yes, it's messy. Blame the swedish pedant working before genes were discovered for it."

Or, less ranty - "In this case, the genetic data tells us there three distinct groups in Prosimii. However, because they all have similar features, we'd like to lump them together for identification and historic reasons. It's clear they don't particularly fit, and in the case of  Lorises and Tarsiers, their grouping is in no way more closely related than Lorises and Lemurs, but this is how we can get things to fit with the existing taxonomy classification

@Lupe: "Taxonomy is a giant sham". Does it matter whether we consider a Texas cougar the same species as a Florida panther (or that there is admixture)? I think it's more important for the public to realize that "invertebrates", "trees", etc are meaningless groupings, while "bird", "bony fish" (with very few exceptions), "insects", "mollusks", "flowering plants", etc are meaningful. Still other words are half-truths: "reptile" excludes birds, but "reptiles+birds" is a clade.

@KevinKostlan was a reason "taxonomy is a giant sham" didn't make it into my answer! Was being a bit factious. But, I think it's reasonable to argue that there are, at this point, such significant issues at every level of the taxonomic model that if it was less well established, we'd chuck it in favour of something better. I think it's important to acknowledge when we talk about it that there are great big holes in bits of it, too, which helps make more sense of its contradictions

These are terms to describe names we give things that don't really follow phylogeny accurately. Fish, for example - a monophyletic group involving fish would include humans, too, yet there are many cases where it's useful to talk about fish without meaning every land vertebrate, too.
From the page you link to:

The term was coined by Willi Hennig to apply to well-known taxa like Reptilia (reptiles) which, as commonly named and traditionally defined, is paraphyletic with respect to mammals and birds. Reptilia contains the last common ancestor of reptiles and all descendants of that ancestor, including all extant reptiles as well as the extinct synapsids, except for mammals and birds. Other commonly recognized paraphyletic groups include fish, monkeys, and lizards.

If you want to use any of these labels: fish, monkeys, lizards, reptiles, it's useful to have a term to describe how those labels relate to phylogeny, hence the term paraphyletic.

The quote seems a bit circular: "paraphyletic was coined to describe taxa which are paraphyletic"?

@terdon I'd paraphrase instead as "paraphyletic was coined to describe taxonomical words already in use". For reptiles, the quote also points out which specific taxa make "reptile" paraphyletic: mammals and birds, which is extra information and not circular.

One very simple example that most people are familiar with is the vernacular use of "animal". Most people recognize that humans are animals and more closely related to other animals than plants. However, usually when people say "animal" in everyday speech, they mean what would technically be called "non-human animals". "Non-human animals" are a paraphyletic group, including the last common ancestor of animals and all their descendants, but excluding humans.
While fish and reptiles are good examples, due to strange tendencies of popular culture, I think that laypeople are more familiar with birds being descended from dinosaurs than mammals being descended from fish. So you could say:

Since all birds are descended from dinosaurs, you could rightfully call birds "dinosaurs", and sometimes scientists do. However, when a five-year-old says "dinosaur", they aren't typically thinking about birds but referring to a paraphyletic group: extinct scaly creatures, maybe with some feathers, but excluding modern birds. Scientists sometimes say "non-avian dinosaurs" to make this explicit.

I put some comments further up, but if I was teaching this, my first attempt would be to "acknowledge the absurdity" - basically, that these groups clearly don't, according to the genetics, fit together.
The next bit is to talk about physical similarities - what features do the creatures share that might make someone group them together?
Then I think we'd talk about how we have two different classifications we're trying to reconcile - traditional taxonomy, which is how the entire body of research we have before genetics is organised, and modern phylogenetics.
Taxonomy groups creatures by physical features, and is broadly qualitative. It is produced by the determination of taxonomists.
Phylogenetics groups by nearest common ancestor, and is based on hard genetic data. However, it tends to ignore large physical features.
Polyphyly is just an area where two groups identified by taxonomy as closely related, share less common ancestry than a group that was not included by taxonomy - it's a taxonomic screwup, but one we can't simply fix. In time, as taxonomy is revised to take into account genetics, it is likely to be resolved, but that takes an extremely long time.

To answer your specific questions

But why not just make the blue area a full blue triangle to make the
prosimii and simiiformes one triangle/group? In the end, we all share
the same ancestor, so I don't see why they are disconnected.

They are one group, called primates.
That is not an image of all the clades for those organisms, it is just an example of the types of groups. Clades can be nested. The link below may help you. Cladistics is a organization of ancestor not just arbitrary categories. A clade is literally often defined as Organism X plus Organism Y, their Most Recent Common Ancestor, and all of its descendants.
Also names for groups have history including decades of published papers refering to them. you can't just change what a name is referring too every time we learn something new. Prosimii may have been thought to be monophyletic at one time, relationships change as we learn more about them. Or it could have been named for the things in one group but not in another, because that was something useful to talk about, like lawless fish. groups have history, a paraphyletic group might all be extinct making relation ships difficult to establish or not important for the characteristic being discussed.

https://evolution.berkeley.edu/evolution-101/the-history-of-life-looking-at-the-patterns/understanding-phylogenies/
Using anything that does not reproduce as an analogy has a big problem, for instance changing what is or is not a planet does not make a prediction about what the origin of all those planets/not-planets are. Cladistics is a map of ancestry and evolutionary history. A paraphyletic group might still be useful if everything in the group is extinct or lives on a different continent, or share similar features. Consider the terms non-human primate, non-avian dinosaur, or non-tetrapod fish, those are groups that are paraphyletic,  but still useful groupings to make for discussion. They are abasically ALL X that do not have feature Z.

I would use reptiles as an explanation. Most people think they "know" reptiles (though they may mistakenly exclude turtles). So tell your layperson that birds are actually reptiles. If you exclude birds, it is just like having some cousins who look very different, so you decide they are not a part of your family! But that would obviously be false. In the same sense, the group 'reptile' is false, since it excludes birds. We call such false groups 'paraphyletic' because it sounds more academic than the phrase 'false group'.
It turns out there are many, many false groups as people were putting living things into categories for centuries before we had readily available DNA sequences.


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How does the SNS increase the heart rate when it causes an increase in cellular uptake of potassium?
Since β-Adrenergic stimulation increases cellular uptake of potassium, this will reduce the plasma concentration of potassium. Thus, a more negative membrane voltage will arise as the potassium ions flow out of the cardiac muscle cells more easily due to the more steep ionic gradient set.
This, consequently, makes it more difficult for an action potential to fire, and as a result, a decrease in the heart rate. So now since the sympathetic nervous system increases the heart rate, then why does this beta adrenergic stimulation occur? It would decrease the heart rate, so what is happening?
This information is from the medical physiology Guyton and Hall textbook, page 384, put into my own words if I have understood it correctly. This is the entire quote from it:
"β-Adrenergic Stimulation Increases Cellular Uptake of Potassium:
Increased secretion of catecholamines, especially epinephrine, can cause movement of potassium from the extracellular to the intracellular fluid, mainly by activation of β2-adrenergic receptors." Or does this mean that the stimulation causes a direct intake of potassium ions FROM THE PLASMA INTO THE CARDIAC CELLS, hence causing a less negative membrane potential and an easier firing of an action potential?
Many thanks in advance!

It's important to keep in mind that extracellular potassium concentration is normally very tightly regulated at 4.2 mEq/L (±0.3 mEq/L in nonpathological circumstances.) It's precisely because so many cells are so sensitive to extracellular potassium levels.

Since β-Adrenergic stimulation increases cellular uptake of potassium, this will reduce the plasma concentration of potassium. [Emphasis mine.]

If this were the case, the entire body would need respond to increased K+ levels, which would present some difficulties. So your second interpretation is the correct one.

Or does this mean that the stimulation causes a direct intake of potassium ions FROM THE PLASMA INTO THE CARDIAC CELLS, hence causing a less negative membrane potential and an easier firing of an action potential?

The effect of receptor stimulation is localized to the cells which have that receptor. So β-adrenergic receptor stimulation causes in increase in heart rate and contractility, whereas β blockers decreases same.
More than I knew and more than you probably want to know at this point abot about β-adrenergic receptors in the heart
One of my mnemonics for β-adrenergic receptors was "1 heart, 2 lungs" to remind me that the heart was predominantly β1 and the lungs β2. β2 stimulation in the lungs decreases smooth muscle contractility, which is why we used to give epinephrine to those with asthma attacks. That's been replaced with albuterol and atropine, but epi is still useful if the attack is severe enough.

Hey thanks very much for your help! So do you mean that the heart does not have as much of β2-adrenergic receptors? But so they still do have some, right? So during for example exercise, the SNS is activated stimulating the β2-adrenergic receptors to cause an influx of potassium, hence causing a more positive membrane voltage, and as a result, the heart muscles are able to contract more easily, increasing the heart rate? Many thanks again!

Yes, they have both, but β1:β2 is about 70:30. If this answers your question, you might consider accepting the answer. Thanks.

okay cool! And so just to summarize it, is the answer to this: "So during for example exercise, the SNS is activated stimulating the β2-adrenergic receptors to cause an influx of potassium, hence causing a more positive membrane voltage, and as a result, the heart muscles are able to contract more easily, increasing the heart rate?" a yes?

Well, it's also linked to CAMP and Ca++, but for the purposes of your question, yes. See the source I linked to for how complex it is, and this was the easier of a number of papers. Most of the papers dealing only with K+ involved the treatment of heart failure... so weren't too helpful.

great! thanks so much!


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D-Galactose effects on primates?
A lot of studies are made using D-Galactose as a accelerated aging model in rats and mice, but why not in non human primates? How much relevant is the galactose rat model for human health perpective? (in the sense that galactose can have similar bad effects in humans)

It helps to support your question with references - e.g. a review paper on use of D-Galactose as an aging model.

Have you any idea how expensive it is to do experiments in non-human primates, and how difficult it is to get ethical permission?  You generally need an extremely strong case relating to concrete high-priority human health benefits. Aging is not that.


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Immunoaffinity chromatography: avoiding damage to the antibodies from proteases
What are the possible methods to prevent the digestion of antibodies (mainly Polyclonal) by proteases during affinity chromatography?
I read some papers about doing modifications to the anitbodies:
using unnatural amino Acids
using mPEG
But, are there better options, more commercially applicable?
I am trying to find a way to purify hyaluronidase from hepatopancreas of red king crab (using polyclonal antibodies). In this case, inhibitors like EDTA, Benzamidine, PMSF don't prevent proteolysis.
These are the Hepatopancreas proteases: (Collagenolytic Serine Proteinase PC (PC—Paralithodes Camtschaticus), Collagenolytic Serine Proteinase PC 2, Trypsin-Like Proteinase A, Chymotrypsin-Like Proteinase C, Aminopeptidase PC, Carboxypeptidase PC, Trypsin PC, Elastase, Cathepsin L, Metalloproteinase)

You need more protease inhibitors, and likely higher concentrations of them too, given that you're working with extracts that are just chock full of proteases. Inhibitor cocktails like this one are available from many companies. Read the specific literature of work relating to this organ or just experiment empirically to determine optimal concentrations.

@MattDMo Thank you, but could there be other methods to isolate the anitbodies from proteases? During/before affinity chromatography?

Protease inhibitors are really the tried and true method of protecting proteins, both the ones of interest in your sample as well as those complexed to the column beads. The problem with trying to modify the immunoaffinity antibodies is that you could very easily end up altering, damaging, or completely destroying their ability to bind to their substrate. That won't happen using inhibitors. I guess I should back up a bit - are you seeing damage to your antibodies, and is there a particular reason you can't/don't want to use inhibitors?

@MattDMo Inhibitors will be added anyway, but I was thinking of other possible ways to reduce  protease activity from the crude extract before starting chromatography. Because in this case, relying on inhibitors won't be very effective, they don't work on all the proteases of hepatopancreas.

The product I linked to (I have no affiliation with the company) has a number of other inhibitors than the ones you're currently using, targeting multiple different classes of proteases. That's what I suggest you look for - a "pan"-inhibitor cocktail designed for working with difficult extracts. As for other ways of reducing activity in the crude extract: you could try using detergents or chaotropic agents, but those will also interfere with antibody/antigen binding, and so I wouldn't recommend them. You could use heat to denature, but again you might interfere with Ab binding.

@MattDMo Thanks!


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How similar are polyembryonic plant siblings to each other?

I successfully germinated all the seeds I found in a Yuzu fruit. From about half of the seeds there are 2 little plants growing, like in the picture. I understand this is due to the occurence of polyembryony, which is quite common in the genus Citrus.
My question: Are the two plants growing out of the same seed more closely related (= more genetically similar) than two plants growing out of different seeds (of the same fruit)?


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What happens exactly in the electron transport chain when there's no oxygen
what is the mechanism of hypoxia in the electron transport chain? It stops because there's no terminal electron acceptor so the IV complex become "stuck" with an electron? There's no other molecule that can accept electrons just like the oxygen?

This article suggests fumarate is an alternative terminal acceptor under low-oxygen conditions

@Aditya thank you.


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What is the area around a plant that is under its phytochemicals/secondary metabolites influence?
Is there a dilution threshold as a function of distance or some general measure regarding the area around a plant that is under the influence of its phytochemicals?
I'm looking for a objective value so I can proceed with a sample of aquatic macroinvertebrates in this area. I know it is something difficult to determine because of n factors, though any general, peer-reviewd information would be appreciated.

Welcome to SE Biology. This question is interesting but currently too broad to answer. Rewording to a specific plant (or group of plants), phytochemical, and aquatic macroinvertebrate (or group) might help.

I was pretending to address the effect of secondary metabolites from the white ginger lily (Hedychium coronarium) on aquatic entomological fauna according to different distances/buffers, expecting to find some threshold for functional diversity or other response variable. This is still an incipient idea that I need to refine.

Your comment has the kind of information that we would need to answer the question, directly including it in the question usually works best for useful answers. Also, you will need to directly @  for them to see your comment. Though that is also not working so well for me here for some reason.


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What is the sequence similarity between humans and chimps in the noncoding genome?
I've seen some papers discuss extensively how human and chimp genomes compare in many of their features, eg Suntsova & Buzdin 2020, but I have not been able to find a paper that specifically studies and determines the sequence similarity percentage between humans and chimps specifically at noncoding regions (of course coding regions are known to have similarity around 97-99% depending on the metric).
So I am curious to ask here: what is the percentage of noncoding sequence similarity between humans and chimps?

If you include a citation it needs to have a full journal reference or a link, otherwise it is of little use.

@David The use is that if you copy/paste the reference I gave into google, the relevant paper is the first search result. In any case, I was just explaining where I was coming from, the paper itself is not relevant in answering my question.

According to "MUMmer4: A fast and versatile genome alignment system" (Plos Computational Biology 2018):
"First we aligned the current assemblies of human and chimpanzee, using the default nucmer4 options with 32 parallel threads ... We used human as the reference and chimpanzee as the query sequence. The human GRCh38 assembly contains 3.088 Gb of sequence while chimpanzee assembly, with 3.31 Gb, contains 7% more DNA. (Note that the chimpanzee genome is far less polished than human, and much of the extra DNA might be explained by haplotype variants or incompletely merged regions; thus the two genomes might be much closer in size than these numbers indicate.)
MUMmer had 2.782 Gb of the sequence in mutual best alignments, where each location in the chimp was aligned to its best hit in human and vice versa, with an average identity of 98.07%. The 1.93% nucleotide-level divergence found here is higher than the 1.23% reported in the original chimpanzee genome paper [25]. Our higher divergence is likely due to two factors: first, the 2005 report was based on 2.4 Gb of aligned sequence from older versions of both genomes, while ours is based on 2.782 Gb (16% more sequence) aligned between the current, more-complete versions of both genomes. Second, the original report used different methods, and may have counted fewer small indels than were counted in our alignments. Approximately 306 Mb (9.91%) of the human sequence did not align to the chimpanzee sequence, while 138 Mb (4.15%) of the chimpanzee sequence did not align to human. We detected 390 Mb in alignments where multiple sequences from chimpanzee aligned to the same location in human sequence and thus only one was chosen as the best alignment based on alignment identity. The genomes are very similar across all chromosomes, with the percent identity varying only slightly, from 97.5% to 98.2% for chromosomes 1-22 and X. Chromosome Y was an outlier at 96.6% identity over 84.6% of its length; however this is likely due to the fact that the chimpanzee Y chromosome is much less complete than the human Y."
A more recent 2020 paper (https://doi.org/10.3389/fgene.2020.00292) found:
"Since centromeres and unsequenced regions correspond to biological features, calculations including N’s and centromeres are listed in parentheses. Initial alignment coverage is 95.57% (90.9%) of the Hg38 reference, and identity within the alignment of 98.65%."
So, it seems that if you include the noncoding genome, the sequence identity between human and chimp genomes is around ~90–91%.

good answer too!


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Confusion regarding the role of the capacitor in the electrical equivalent of a membrane
I am having trouble understanding the electrical equivalent of a cell mebrane as it is shown in this picture taken from Kandel:

What I cannot understand is the capacitor in the specific image. Why is it set parallel to the resistances and what does it symbolize? Does it symbolize all the charges that are accumulated in the cell border? What does the derivative of its charge $\frac{dq}{dt}$ that is shown in the relation $C=\frac{q}{V}$ mean? From my point of view the capacitor symbolizes the two sides of the membrane and so the derivative mentioned above should be equal to the total current through the membrane. However this is my personal opinion that I have not confirmed and which contradicts the electrical equivalent given above. Can someone give me some help?

Please ask one question at a time. Right now the answer to your question would be a chapter in a neurophysiology textbook (seems like you should have one in Kandel). What does it teach you?

@BryanKrause I have the  Jessell, Thomas M.; Schwartz, James H Principles of Neural Science. My problem is not related to what the book sais but to the physical  interpretation of all these membrane properties.

Okay; I think if I am understanding your questions correctly the first and last have already been answered here, and your middle question isn't really about biology but just physics and what capacitance means. Have you searched for these answers? If you can't find one, then still please ask individual questions supported by what you know about each.

@BryanKrause I edited my question in order to refer to a single topic. I cannot understand however what do you mean that the first and last questions have been answered. I don't see any answers.

Did you use the search to look for existing posts on the site? That's where you would find answers.


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Is there a word to describe a sample of DNA that can be sequenced?
This is a question about terminology. I want to know if there is a word that is used to describe a sample as "able to be sequenced".
My rough guess would be "sequencable". But that does not seem to be a word. "Viable" would be my second guess. But seems to imply a lot more than that it can be sequenced.
What is used in practice?

As always with adopting general English words to scientific use, the exact context is crucial. What do you mean by the opposite “unable to be sequenced”? Do you mean the DNA is too degraded or has been converted chemically through age, do you mean it is contaminated with DNA from bacteria etc, or do you mean it is one of many repeats?

But if you change your spelling to "sequencEable" you'll find that it was entered by someone in Wiktionary in 2019 (https://en.wiktionary.org/wiki/https://en.wiktionary.org/wiki/sequenceable). Apparently it has been used in a mathematical sense for many years (https://books.google.co.uk/books?id=UywypI5sjvgC&pg=PA253&lpg=PA253&dq=sequenceable&source=bl&ots=uOkYs-DZ1j&sig=ACfU3U271_SuaKnQ6PqdoSHYRFdHjTq_YQ&hl=en&sa=X&ved=2ahUKEwjezLGx06n9AhWFSMAKHZhkBy8Q6AF6BAgiEAM#v=onepage&q=sequenceable&f=false). A Google search for "sequenceable DNA" finds it in Scientific American.

@David is correct; sequenceable is definitely a word; it has been used in the biological sciences for quite some time now. I can find published papers using the word dating back to 1996, so probably earlier than that even.

I think you should request migration of this question to the English language Stack. It's off topic here I think, but definitely on-topic there.

I'd just delete the question, given the trivial nature of the answer. As a regular user of SE English Language and Usage, I don't imagine they would think much of it.