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Is there a minimum amount a muscle can move? And thus, gaps in our movement?
Lately I've been thinking about something, based on my knowledge my chain of reasoning works like this...
When you want to move a muscle your brain sends an electrical nervous impulse along the chain of nerve cells to the muscle you want to move.
A nervous impulse is nothing other then a jolt of electricity, the voltage is uniform and the only difference is the rate the jolts are sent, resulting in faster movement.
When a muscle is hit by electricity it's reaction is to contract, this is what creates movement.
Given all this, is our movement continuous or quantized? Let's say one jolt moves my finger 1 degree, another jolt would move it another degree. Would that not make it impossible to move my finger 1.5 degrees? To me it stands to reason that while you could shut off the power to your finger at any time, making it theoretically continuous, there must be a minimum amount of frequency by the impulses needed to cause any movement.
If this is true then the movement of our bodies is the microscopic snapping through possible positions. And therefore there must be a finite number of possible positions our bodies can take. Like a knob that can only click it's way through the pre-determined positions on the dial.
Is all this true? Do nervous impulses work like I think they do? Are there things about nervous impulses or muscles we don't know? Are we capable of only positioning ourselves in this quantized way? Has anyone proven any of the things I have said? Please consider you answer carefully.
Personally I hope our ability to position ourselves is continuous.

That's not even close to how muscle signals work, you may want to look up something called muscle recruitment or muscle fiber recruitment.

What about the rest of my question?


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Does the nature of nervous impulses give us a finite number of things we can perceive?
This is a subject that is very disturbing to me and one that I've been obsessing over for years. I warn you now that this is probably not the sort of thing you get asked on this website and I'm not even sure if I'm explaining it very well but please bear with me.
I have, or at least used to have, a great passion for art and have always been a very creative person. But years ago I began obsessing over the idea there are only a finite number of possible images that we can perceive. And therefore everything I have ever created or will ever create is part of a predetermined, limited set of possibilities.
The amount of knowledge I have about how perception works is that when light hits a photoreceptor in the eye it fires electricity into its connecting nerve cell, this triggers the nerve cell to zap the next one and so on until it reaches the brain. The brain has a memory of where each chain of nerves is connected to and so it identifies that otherwise indistinguishable zap as coming from a particular photoreceptor in the eye. That each chain of nerve cells simply transmits it is on or off and nothing else. I worried that meant our perception works exactly like am LED screen, meaning that when light shines on the grid of photoreceptors, the image that gets sent to the brain is made of dots of exactly one solid colour and the only reason we don't notice it because the brain smooths the edges. This would mean that, if eyesight works like a digital camera there is a finite limit of things that we can possibly see because there is a finite number of images you can possibly create with a digital camera.
I even found an article on the Internet that claim that's exactly how it works, they even have a diagram:

Eventually I found a way around it when it turned out that the eye is constantly making microscopic movements even when holding still.
But what about hearing? I know we have sensors in the form of hairs that trigger a nervous impulse to the brain when they are stimulated. But as I understand it, each one can only send that on/off binary signal when they are triggered by a very specific level of sound. What happens if there is a sound that is in between two hairs? Do you simply not here it? Is the same true for all the sensors we have?
I know that the brain processes a lot of what is sent. I know that there are things outside our range of perception such as ultrasonic and UV light. And I know we all have our personal reactions and even perceptions. But none of that matters to me.
What I want to know is, can our senses cover a continuous spectrum? Or, is everything we perceive a number of discrete and finite possibilities made up of digital, pixelated, quantised information? Can we only perceive image A and image B with nothing in between, or can we perceive image A.012744 and A.064212454 And A.24545157845?

I know we have sensors in the form of hairs that trigger a nervous
  impulse to the brain when they are stimulated. But as I understand it,
  each one can only send that on/off binary signal when they are
  triggered by a very specific level of sound.

Your overall question borders on philosophy and the biology of consciousness which is hardly understood at all. However, your picture of sensory input is a huge oversimplification. That's not really your fault, it's the sort of thing you are likely to pick up from pop science descriptions, which in turn are faulty because this is not a dead field where everything is understood to a T. Even the question of which parts of perception "are" digital and which "are" analog is still under investigation. However it makes your question hard to answer because it's sort of ill-posed since is assumes a purely digital model.
To address one oversimplification, our perceptions of the outside world are not necessarily binary on off bits. It is hypothesized that some neurons signal by changing the rate at which they fire. Is the rate continuously variable? It's not clear, but it certainly provides a much larger range of encodings than 1 and 0.

Can we only perceive image A and image B with nothing in between, or
  can we perceive image A.012744 and A.064212454 And A.24545157845?

I don't know how this meshes with your statement that 'And I know we all have our personal reactions and even perceptions'. If you've ever looked into color blindness then you already know that some of your fellow humans can't distinguish between A.012744 and A.064212454, even if you can. It's not that they can't see them, they just can't tell that they are different.

Correct a digital model is just all wrong for the brain not because a neuron is not digital (it is) but because the signal from one neuron to another is not. Due to how neurotransmitters and inhibition interact. A neuron is on or off but the signal from one neuron to another can have a variety of states. The closest electronic analog is a memristor.

I have already read that the frequency of spikes denotes the intensity of what is being sensed. But frankly this doesn't answer my question.

Here's how I understand eyesight works: imagine a control room inside the brain, one that has a screen made out of light bulbs, each bulb capable of only displaying one solid colour. As I understand it, when light hits the photoreceptors in the eye, the electricity passes along the chain of nerds and makes that lightbulb turn on because that's the one it's connected to. The lighting and colouring of these bulbs generates the image we see in our heads.

What bothers me is that there is a highly quantised nature to this image, there are real-world details that escape the process because they are in between the photoreceptors/light bulbs. Sort of like trying to view the world through a colander or a grill.

Is that how eyesight works? Does it work like in the diagram I posted? Do we not know a great deal about human perception already?

I've spoken at length to someone I knew about this (although he wasn't an expert in this field) he was very insistent that the brain could do all kinds of things with the information received and that made our visual possibilities infinite. I strongly counter argued that I was talking about our ability to perceive the real world and that depended on the information we are capable of receiving in our brains.

Recently I felt a little better about this problem because I read that our eyes are constantly making microscopic movements even when we are staring at a fixed point, that would allow our eyes to fill in the gaps. But then I thought about hearing, the senses in our ears are still discreet and quantised and ears don't constantly move around. Aren't they then bound by the limitations I've already described?

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How to calculate the quantification of qPCR to the equivalent of the number of nuclei in fungi?
I have a question about the quantification through qPCR. The my question is: if I made the qPCR of a fungal functional gene, how is possible to obtain from the quantification number (in nanogram) the equivalent number in number of nuclei?

To clarify: you're asking about converting between copy number (which may be expressed in moles, molarity, or just a raw number) and nanograms of DNA?

If I obtain the quantification between nanogram to covert this number in number of nuclei. Because in one paper I found this sentece: "As few as 148 fg of Verticillium dahliae DNA were detected and quantified (through qPCR), which is equivalent to five nuclei". How is possible to make this convertion? @Punintended

From your comment:

"As few as 148 fg of Verticillium dahliae DNA were detected and quantified (through qPCR), which is equivalent to five nuclei". How is possible to make this convertion?

The Verticillium dahliae JR2 genome is 36.2 Mb.  Assuming this organism is haploid and dsDNA has an average mass of 660 g/mol per base pair, that means the molar mass of the genome is 2.40 × 1010 g/mol.  Therefore, 5 nuclei will contain 8.30 × 10-24 mol of your genome.  Multiplying the molar mass by the number of moles gives us a mass of 1.99 × 10-13 g, or 199 fg, which is close to your cited value.

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Frog bloated with pool water
I found a gray tree frog in pool skimmer basket, he seems quite alive but terribly bloated with water. I tried holding it upside down a bit to see if some water would come out but only a few drops. Any ideas if there's anything I can do, or just let nature take it's course maybe he'll survive if given enough time without predators (cats and birds and whatever, around here in Ottawa Ontario).

I have no expertise in this, but it could be the pool chemicals were absorbed and caused this, and if so allowing it access to a large amount of fresh (nonpool) water might give it the best chance to survive.

I'm voting to close this question as off-topic because it is trivial. This site is for academics, researchers and students of biology. It is not an animal rescue society.

I can't say if the question is trivial but there can be multiple possibilities for why the frog is bloated. Unless you provide some additional details providing a conclusive answer would be difficult. However, it seems that the frog is affected by chlorine in water. Nonetheless, we consider personal medical questions and health advice for both humans and animals, as off-topic.

Most frogs die in minutes in chlorinated swimming pool water , after some time they will swell with gas. I have pulled toads out of pools and they have survived ; I assume their dry skin is less permeable to pool chemicals than frogs.

The pool is salt based, i.e. you don't usually smell chlorine after swimming. And the only chemicals in it were a bit of shock a couple weeks ago to kill the algae, and based on the water sample yesterday, that's pretty much dissipated so maybe its not so bad.


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Do mRNA vaccines encoded proteins get glycosylated?
per recent hype around the new mRNA vaccine against COVID-19 (or sars-ncov-2) it got me thinking about the mRNA vaccine principle.
From my biochem education I've taken, that human proteins are usually glycosylated.
It got me thinking, that if the mRNA vaccine encoded proteins would be glycosylated by human post-translational machinery, would present different epitope then the not-glycosylated one.
While I understand that the polyclonal antibodies target a lot of different epitopes, it seem to me that the performance of antibody protection obtained in such way could be limited.
I've researched this a little bit and there seems to be techniques to avoid the glycosilation machinery.
My questions in essence are:

Would proteins encoded by mRNA vaccines get glycosylated (if not mitigated)?
If yes, then do the vaccine designers use some methods to bypass the glycosylation?
If yes and no mitigation has been implemented, do we just count on chance that at least some part of protein surface to present the same epitope as the original target protein?

Found sources:

https://www.nature.com/articles/s41581-019-0129-4
https://www.pnas.org/content/117/3/1280
https://en.wikipedia.org/wiki/Glycosylation

Please forgive me my English and any typos. :)

@tyersome Thanks for the pointer about the viral proteins origin - I've totally missed that.

Your memory of your biochemical education is faulty. Only certain proteins are glycosylated — those that pass through the Golgi. And if you think about it, if you deliver a mRNA to the cell, it’s fate should be exactly the same as if the virus had delivered it. Perhaps you should.


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What could cause individual false positives in ELISAs, while the rest of the plate looks fine?
I run indirect ELISAs for COVID antibodies. That's my whole job right now as a research technician. I coat the plates with a pure RBD, then detect antibodies in serum. Recently it's come to light that I've run plates with false positives. Running those same serum samples again gives VERY different (negative) results. If entire plates were giving false positives we could figure out what mistakes I'm making, but for the most part the duplicates look good, the standard is good, the dilutions are good... The person who wrote this protocol hasn't included a negative control because there have been occasions during the development of the protocol where pooled serum from 2018 or earlier was used as a negative, but those pooled serum controls were somehow consistently more positive than that of several confirmed, post-recovery COVID patients. Obviously that lack of negative control has predictably come back to bite us.
Originally we thought it was a plate washer malfunction, but it turns out these smatterings of false positives predates the plate washer acting up.
The short of the long is that some of my plates have very clear, obvious negatives, some borderline positives, and some clear, obvious positives. The issue is that some of those positives are false positives and neither I nor my supervisor can for the life of us figure out why.
Ideas would be awesome. ELISAs are my entire job right now, and the PI is understandably not thrilled with me.
Additional details:
Plates are washed by an automatic plate washer after the incubation of sample dilutions, and after the incubation of the secondary antibody/HRP. The plates are blocked before sample addition with a fractionated bovine serum/gelatin/tween20 blocking buffer. Dilutions are made in that same blocking buffer, and the secondary antibody is also diluted in blocking buffer. We're using Immulon 4HBX plates. The plates are developed with ABTS in McIlvain's plus H2o2.
Ask my anything else that might help figure this out. I'll answer what I can.

Is your detection or secondary antibody aggregating? I've done extensive clinical ELISA development in the past and when this problem inevitably crops up for these assays the most likely culprits in order were:

Plate washer acting funny
Antibody aggregates binding nonspecifically to the plate
Inefficient blocking reagent/not enough time spent blocking
Person running the samples is mixing things up

Even if your false positives predate the platewasher malfunction, you could still have a leaky/clogged dispensing nozzle. Try rotating the plate 180 between wash steps or hand-washing and see if that helps.
For aggregated secondary/detection ab, give them a brief spin and pipette off the top, and for blocking increase volume/time.

Sympathy...
Quite possibly the samples change over time.
The antibodies your test selects for may be reacting in the messy biological sample.
If it were possible, grab the people giving the interesting samples and get a PCR test on them to see if they are positive or not.
An experiment on the effect of waiting time on the samples would be interesting, it might be nice if it were performed at another lab to reduce your stress.
I hope your discovery gets you cited in relevant research or industry publications.

Thank you! We collect saliva as well with each visit to check for active infection. I'll bring up the idea about the antibodies reacting in the sera and waiting time. This is my first tech position post-undergrad, and I love it very much so I want to do the best I can. Thank you again!


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What kind of house plant is this?

This is a house plant I have that I love but I don’t know what it’s called. I’d love to research it and even buy more but it’s name is a mystery. Picture taken in Ontario, Canada.

IMO, this question would be a better fit on gardening.SE.

It looks to be a Clivia; The English common names are Natal lily or bush lily.
It's a plant that comes originally from Africa but it now commonly sold as house plants.
The Wikipedia article give a good information about that plant.
Example:

Picture taken from this site.
You have also to notice this is a toxic plant and to keep away from small children or pets.

For downvoter(s), please explain why my answer is not good and how it can be improved? If you think it's wrong, please just tell what the good answer (and post it as well).

not sure about the down votes, but maybe you could add a good description or image to show the similarities between the Clivia and the plant in question.

I added some more details as requested. If someone have a better answer I would delete mine without problem.


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probability of hairpin vs self-dimer formation?
I have a linear ssDNA oligo that is designed such that the ends are complementary, and conducive to hairpin formation (see attached figure). My question is, which has a higher likelihood of formation, a hairpin, or a self-dimer? Would the likelihood of hairpin formation increase if I decrease the concentration of the ssDNA oligo during the annealing process? If I enter the sequence in IDT oligo analyzer, the gibbs free energy for formation of self-dimer is significantly lower compared to hairpin.
The melting temperature of the complementary part of my oligo is 50 deg. The annealing will be done in nuclease free water, without any Mg+.

I have tested a similar design to this. With a duplex protocol the chance of forming a hairpin is much higher than that of forming self-dimer, even at concentration of 25 μM. You can run a 3-5% agarose gel to test the outcome.

Welcome to SE Biology. Your answer sounds reasonable but we have no way of judging whether it is correct for lack of evidence. Do you have your own gel to illustrate this?


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Osmosis/ Facilitated diffusion
Water can move across the (Semipermeable non polar lipid) membrane by simple diffusion (osmosis).
But polar molecules cannot pass through the non polar lipid bilayer, they require carrier proteins to facilitate their movement.
But water as well, is a polar molecule. How and why does it simply pass through the non polar lipid bilayer by simple diffusion and not by facilitated diffusion (i.e., through carrier proteins)?

@user1136 If you have an answer it should be posted as an answer rather than as a comment.


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Immunological factors for the cause of headaches following SAR-CoV-2/COVID vaccination
It is generally-accepted that headaches are a common side effect from receiving the COVID vaccine.

Vaccine recipients with pre-existing immunity experience systemic side effects with a significantly higher frequency than antibody naïve vaccines (e.g., fatigue, headache, chills, fever, muscle or join pains, in order of decreasing frequency, P < 0.001 for all listed symptoms, Fisher’s exact test, two-sided).

— Florian Krammer et al.: "Robust spike antibody responses and increased reactogenicity in seropositive individuals after a single dose of SARS-CoV-2 mRNA vaccine" doi: https://doi.org/10.1101/2021.01.29.21250653
I am trying to understand why. What theories or known biological, immunological or otherwise physiological mechanisms would cause recipients of the vaccine to report headaches as a common side effect?

Headaches are a side effect of both vaccinations and infections.  Have a look at the effects of cytokines, particularly Interferons.

Headache is one of the various side-effects of vaccination. Typically, a person will have pain in the site of injection, muscles throughout your body and head.
The immunological reason is the network of our immune system. Whenever a foreign antigen (vaccine) is detected by our immune system, antigen-presenting-cells (macrophages, dendritic cells) takes the antigen to nearest lymph nodes where it is presented to the adaptive immune system. Due to this invasion, strong immune response starts which leads to the pain.

Image Source: wikipedia.org/wiki/Lymphatic_system

Thanks for the amazing answer @Riq (I would upvote you +1 but I don't have enough rep!) -- one quick followup question for you, if you don't mind. It sounds like you're saying that when cells, such as macrophages, present lymph nodes with antigens (from the vaccine) this initiates an immune system response, which you say leads to "pain". But why headaches? Why is this pain so specific to the head? Thanks for any clarification!

BTW I am not the one who gave you a downvote! I am happy with your answer so far!

@IamYourFaja You can accept the answer if you think it answered your question.

Yes thanks again @Riq, do you have any ideas regarding my followup question above ("But why headaches?...") Perhaps something to do with the cytokines and interferons that Polypine mentioned?

@IamYourFaja yeah, cytokines are essentially the communicator of our immune system. They help in cell signaling and involved in various side effects of our immune system. Hope this clarifies your follow-up question.


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Effects of a constant magnetic field on the human body (especially blood circulation and ion channels)?
Recently, while searching for the safety of MRI, I read in several places that hemoglobin and iron in the blood are not significantly affected by magnetic fields, so MRI is safe.  However, since the human body contains many kinds of metal ions, I'm wondering what effect would the long-term exposure to magnetic fields have on the human body, unlike in the case of MRI.

You might be interested to see the video of a frog levitating due to the strong (inhomogeneous) magnetic field. This experiment earned its authors the Ig-Nobel prize... just a few years before they received the real Nobel for discovering a way to obtain single layers of graphene: https://slate.com/business/2014/05/nobel-prize-in-physics-andre-geim-went-from-levitating-frogs-to-sciences-highest-honor.html


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What is the criterion for genetic similarity among siblings and humans in general?
I just started reading Blueprint by Robert Plomin. He makes some well-known statements about genetic similarity which we all have read somewhere but I would like to know what the criteria for genetic similarity actually are:
He writes that all humans are the same for 99% of the 3 billions base pairs of our DNA. I take that to mean something like this: If our DNA had only 100 base pairs and we compare two individuals, those two individuals' DNA would differ in only one place out of the 100 base pairs.
But he also writes that siblings are (on average) 50% similar genetically. I know the rudimentary story of two chromosome pairs, one from mother, one from father, etc. My question is simply how this can be spelled out precisely. I mean, if any two humans are 99% similar in terms of their DNA, how can two siblings be only 50% similar genetically?
I have a slight suspicion: 99% similarity between the DNAs of any two human beings leaves out 30 million base pairs where they are different. Two siblings then are, in addition to the 99& similarity in base pairs, also 50% similar regarding the remaining 30 million base pairs. Thus, two siblings differ from each other in only 15 million base pairs. SO the 99% shared DNA is what makes us human, as opposed to apes, and the rest constitutes the arena in which individual differences take place?

You seem to have the right idea — 99.5% identical base-pairs rather than 90% — but precision is the key here. X% similar means nothing. X% identical likewise unless it is stated precisely what is being compared. What does the author say precisely, or does he not?

you may be interested in these related answers: https://biology.stackexchange.com/questions/1981/how-many-genes-do-we-share-with-our-mother https://biology.stackexchange.com/questions/61147/neanderthal-human-genetics https://biology.stackexchange.com/questions/61206/how-can-someone-share-50-of-their-dna-with-their-parents-yet-all-humans-share-9?noredirect=1&lq=1

Your slight suspicion is close to correct. There are two different ways to discuss 'proportions of shared DNA' (identity by state, versus identity by descent). If two individuals share an allele that is identical by descent, it must by identical by state, but the reverse isn't true.
The 99% figure comes from comparing all of the base pairs and follows the concept of 'identity by state', where 'state' is A, T, C, or G. If individual 1 and individual 2 both have an A at position 39, they match. Average over all positions in the genome, and there's your 99% figure.
The second part of your suspicion is not quite correct, largely because of assortative mating and drift within local populations. The 50% figure comes from classical theory of Fisher, Haldane, and so on. They were trying to solve the mathematics starting from pedigrees and Punnett squares. They didn't have access to the high-throughput DNA sequence data that is common today, but you can follow a rare allele through a pedigree if it causes some observable outcome in its carriers. As a consequence, the classical theory is defined in terms of 'rare' alleles and follows the concept of 'identity by descent', and is tightly linked to the sorts of things you can observe in a pedigree. Having examined many pedigrees, you can generalise the patterns to derive classical population genetics theory. The key thing to remember here is that this branch of theory is expressed in terms of limit formulae: 'as variant A becomes rare, statement Y becomes closer to true'. In that context, the 50% figure is approximately the probability that your full-sibling has a rare allele, given that you have it.
That 50% is a direct consequence of the mechanics of meiosis: you have two copies of each allele. One copy of each allele was inherited from your mother, and the other from your father, at random. As a result, offspring have an exact 50% chance of inheriting any rare allele carried by one of their parents, and so are exactly 50% identical by descent to each of their parents. By the same reasoning, individuals are 50% identical by descent to their full-siblings, on average. In contrast, all humans are 99% identical by state, because a large portion of the genome is shared by all humans.

I think that your formulation in terms of IBS and IBD is probably the most useful for asker, e.g. "All humans are 99.9% identical by state in terms of aligned DNA sequence, whereas sibs are on average ~50% identical by descent from their parents, in terms of inheriting the same chunk of DNA." I think it's worth emphasizing the motivations between those 2 numbers. Otherwise I very much agree with you, I would just weight it differently.

Thanks! I've just edited to try to highlight that contrast.


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How do APCs find their specific T-cells in the lymph nodes?
My understanding is that when an APC (more specifically a dendritic cell) encounters an antigen in the periphery, it ingests it and presents it on its surface. It then migrates to lymph nodes to activate the T-cell that has the specific receptor for this antigen.
Now, I know that T-cells circulate throughout the body, but given the amount of the cells in a lymph node, and the fact that only a few T-cells are specific for a given antigen, it seems to me highly improbable for the APC to meet the specific T-cell.
Is it really that the APCs randomly check every T-cell there? If so, do we know how long would that take? Or is there a way to quickly locate the specific T-cell?

Can you give some link to Janeway's which is available online or any other reference? - I think it might be some misunderstanding to assume that ther is only one singel (stem) T o B cell that fits. I think it's a "bunch" of stem cells that shares one specifity, so chances are not that bad, to meet.  What's more, there might be polymorphy, i.e. several affinities that fit. Wonder if  you ever came across such or similar argument.


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Do jellyfish have extra energy reserves for emergencies (a "fight or flight" response)?
My friend is writing a story about jellyfish, and we couldn't find out if jellyfish have the equivalent of a "fight or flight response" or an adrenaline rush. In other words, do they have reserves of energy which lets them do things they wouldn't normally be able to (such as surpass harder obstacles, or move faster even when exhausted) which only get released during emergencies?
I know that jellyfish have a distributed nervous system and no brain, but searching the web for "adrenaline rush" and "fight or flight response" only returned results about how adrenaline/epinephrene is a cure for jellyfish stings rather than speaking about equivalent phenomena for jellyfish themselves.

Side note: This comprehensive article in Current Biology mentions something called "escape swimming":

One of the most extensive studies of the neuronal mechanisms of jellyfish behavior has been done on the control of swimming in the hydromedusa Aglantha digitale. Atypically for hydromedusae, Aglantha has two different swimming modes: slow swimming and escape swimming. Slow swimming is their normal mode, and is mediated by relatively regular and weak propulsion of the bell governed by pacemaker neurons in the nerve rings. Escape swimming produces a much stronger contraction of the bell, and is triggered when one of the giant neurons in the nerve rings (ring giant) is excited by mechanical stimulation of the tentacles

This is more related to neuronal impulses than energy reserves, but perhaps escape swimming bears some relation to energy reserves as well (if that's something that exists for jellyfish)?

This paper, Passive energy recapture in jellyfish contributes to propulsive advantage over other metazoans (pdf is freely available) might be of interest. It includes the following "Medusae can exhibit such low respiration rates due to the large proportion of metabolically inactive tissue during swimming. Jellyfish have low body carbon relative to other swimmers, which results in ≤1% of the body mass represented by muscle. Fish, in comparison, have a body mass that is ≥50% muscle" and much more.

Interesting! I'm beginning to suspect there's no concept of an energy reserve for them, if their energy use is already so low anyway (not to mention the passive energy recapture described later in the link).

Search for glycogen and jellyfish (or whatever the proper word for the beasties is). Idly playing I found a paper that implied it was present. I would find it hard to believe they do not build up energy reserves — lack of information does not mean it doesn’t exist. What stimulates breakdown is a different question.


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How do you determine "in which direction" DNA is shared between groups of people
In popular DNA ancestry tests you can read lines like "you have 2% neanderthal dna" or "you have 20% italian". How can you distinguish between a person having 20% italian vs italians having 20% of your dna.
Like if we bred with neanderthals, that means neanderthals would have some of our DNA, but that wouldn't mean that we would have some their neanderthal DNA. Is this reasoning true? Is it possible to distinguish and does this apply to modern groups of people aswell?

The two cases are slightly different.
'Ancestry proportions', such as those given by 23andme, are given in the context of a reference panel. This means that they aggregate genetic data from individuals into particular countries, say Spain, Italy and France. They would then look at the genome of the individual they are testing, and find how much of the genome most closely matches individuals from any of the 3 reference populations. So an individual from the U.K. may share 70% of their genome most closely to the French reference individuals, 20% most closely to the Spanish and 10% most closely to the Italian. These proportions will change if we use different reference panels. In this case, the proportions only make sense in the context of which reference populations have been used. This information is available on here.
Humans have around 2% Neanderthal DNA because (we think) a small group of less than 10 Neanderthals mixed with the ancestors of all extant modern non-Africans. This Neanderthal ancestry was then propogated throughout all modern non-Africans today. The first human - Neanderthal hybrids would of course have been ~50% human and ~50% Neanderthal. However, because the effective population size of humans was much larger, the Neanderthal ancestry became diluted over time. If some early Neanderthal hybrids had then moved back into a population of only Neanderthals, they would have carried with them the human ancestry and we would say that Neanderthals contain x amount of human ancestry. However, as far as we know, this didn't happen and Neanderthals relatively quickly died out.


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Please identify this bone found on the beach
I've found it on the beach in Çanakkale, Turkey. Width 7.5 cm, height 5 cm. Inner hole dimensions are 2.5 cm x 3 cm.

It's an atlas vertebra from a large herbivore, a goat, a young horse, a deer. Also know as the C1 vertebra it's probably a sheep from a mechoui party.

Thank you. Goat is most probable animal here on these beaches.

Hehe look at the moderators joke comment.... " A sheep is an animal which says 'mehehehe' and it's white and wooly"


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How many mRNA strands are in a single dose of the COVID-19 vaccines?
I realize there are several different mRNA vaccines. I would be happy to know the ballpark figure for any of them.
As a follow-up, is it known about what percentage of injected mRNA strands are successfully translated into proteins?

Check https://meta.stackexchange.com/questions/66377/what-is-the-xy-problem - it seems like this question and your other recent question might suffer from this issue. What is motivating the questions you're asking here? What are you hoping to get from these numbers?

Partly it's pure curiosity. I couldn't find this information anywhere. Regarding my other question, after a night's sleep I realize mRNA must be translatable more than once, or it would not be possible for a virus to replicate more than one copy of itself. Still, what about "friendly" mRNAs? What prevents an mRNA from being translated indefinitely? I'm just curious!
But yes, you're right that I am also wondering about how the total number of spike proteins generated by an injection would compare to those encountered in a natural infection.

I think it would be better to ask one of those intended questions more directly, rather than the one you asked - that's kind of where the XY problem comes in where you are asking something that you think will get you closer to answering your intended question, rather than starting with the intended question.

Thanks, I appreciate that. But I'd also just like to know the answer to this question. For what it's worth, I think it would add value to everyone to be able to search for this specific question and find a simple answer. Maybe I'm just searching with the wrong terms, but I was not able to find it.

Well, we can work this out empirically.
We know that the average molecular mass of a base of a RNA is 339.5 g/mol.
Despite this, to calculate the approximate molecular mass of a single-stranded RNA molecule, you multiply the number of bases by 320.5 (because some bases are more common in sequences than others) and add 159 (same source). This means for a single-stranded molecule of 1000 bases, it will have a molecular mass of 320,659 g/mol. The Pfizer vaccine has a sequence of 4284 bases.
4284 * 320.5 + 159 = 1373181 g/mol.
The Pfizer vaccine has 30 ug/shot (PDF, see page 27 under "Description") or 30x10-6 grams
number of moles = mass/molar mass.
n= 30 x 10-6 grams/1373181 g/mol
n= 2.185 x 10-11
number of molecules = n (above) x Avogadro constant (6.022 x 1023)
Number of molecules = 1.316 x 1013
Now this is a ball-park figure because the RNA isn't actually RNA it has had some special additions to the uridines that make it less susceptible to immune regulation, replacing the uridines with  1-methyl-3'-pseudouridylyl (see Wikipedia link to structure above). However, I believe this alteration to the mass, will not alter the number substantially; it'll still be in the 10 trillion range.

The 30 mcg/dose in the Pfizer pdf indeed refers only to the RNA. The lipid nanoparticle etc. is counted separately. In case anyone else was wondering that.

Wow, thank you, @bob1! That is a truly tremendous number. So that would mean that, seeing as we only have 30-40 trillion cells, depending on the uptake of the mRNA into cells and the number of times each strand is translated, you could end up with more spike proteins floating around your body than your total number of cells. What an incredible surface area for your immune system to notice. Awesome!

Also, for comparison, this source (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7685332/) says that at peak infection, a person can have 1 billion to 10 billion virions in their body.

@BrianRak - The data on how much is produced is proprietary. I suspect that the 30 ug is the amount of RNA, definitely not all of that will be packaged, some will be lost to degradation (transport, preparation etc), and some proportion won't make it into cells. My experience using plasmids and liposphere preps (common in bio labs, but not the same as the Pfizer ones) is that somewhere between 30 and 90% of cells in a dish will be transfected, but it will definitely be less than that in vivo. There are too many variables to answer the second part of your question in the OP.

@BrianRak to address your second comment - in culture (ideal conditions) you get about 10^6 (1 million) - 10^7 infectious particles/ml, so these numbers seem surprisingly low to me, but I guess it will be a staged infection - not all cells getting infected at once, unlike in the lab where a whole flask of cells will infect at the same time.


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What is the probability of having a son with blood type O?
So I was solving some biology questions, and this question left me confused. The response is supposed to be 22% according to the answers, but all the methods that I used did not lead me to it. I really hope that somebody can help me with it, the question sounds as follows:
Human ABO blood type is determined by two genes (H and I). First, the H gene codes
for the antigen precursor. The dominant allele (H) leads to expression of the precursor; the recessive
allele (h) does not. Second, the I gene has three allele forms, IA, IB and i, and determines blood type
(A, B, O or AB).
A male with blood type A and a female with blood type B marry. Each of them is heterozygous for
both the H gene and the I gene. What is the probability of having a son with blood type O? Give your
answer as a percentage (%) rounded to an integer (without any decimals).

7/16 for any child to be blood group O, half of that (21.875%) for a son with blood type O.
P  x  M
HA    HB
HO    HO
hA    hB
hO    hO
HA = 0/4 blood type O
HO = 2/4 blood type O (HO-HO, HO-hO)
hA = 2/4 blood type O (hA-hB, hA-hO)
hO = 3/4 blood type O  (hO-HO, hO-hB,hO-ho)
= 7/16 chance of type O
son = 1/2
Chance of blood group O = 7/16 * 1/2 = 7/32 = ~0.22
Edit: as it's not clear from the question, anyone who has genotype hh is not able to express either A or B antigens, so is always blood group O.

Welcome to the site, Greg. I wanted to make sure you're aware of the homework policy on the site: https://biology.stackexchange.com/help/homework For homework questions, we want to make sure people are providing their own reasoning and work and that answers to these questions are about explaining the approach someone might take to a problem rather than answering it for them. Otherwise there's a high risk that people will ask questions here just to get the answer and won't really learn from it.


text:
Why is double stranded DNA considered to be one molecule?
Wikipedia, for example, refers to DNA as "a" molecule, not two separate molecules forming a double-helix structure. Isn't this technically incorrect? There are two separate polynucleotide strands (each that can be considered one molecule on its own as the monomers are joined together by covalent bonds), and the strands joined together by hydrogen bonds and not covalent/ionic bonds along their length. Doesn't that exempt them from being considered one molecule, as the bonds joining them are intermolecular and not covalent or ionic?

If we considered a double-helix to be two separate molecules, then how do describe two separate double-helices? I think using the singular "molecule" with a double helix is appropriate because it makes it easy to use the plural "molecules" when referring to a group of DNA double-helices. Also, there are other supramolecular complexes such as Catenanes and Rotaxanes which are generally referred to as singular molecules despite having no covalent bonds between the parts.

DNA is a molecule. dsDNA is a supramolecular structure. Wikipedia is not the authority on biochemical nomenclature. You can edit Wikipedia to correct this.

I'm voting to close this question as off-topic because it is about the correctness of a wikipedia article. The question may also become invalid if wikipedia is corrected.

Also, it is a possible duplicate of https://biology.stackexchange.com/q/66343/3340

Wikipedia was just an example. The answers to the question linked seem to say that DNA is one molecule. The text referenced in Charles' answer (Molecular Biology of the Cell) says one, single DNA molecule is 2 polynucleotide chains, just like Wikipedia. I find the answer abut DNA being a polyatomic ion/2 polyatomic ions to be the most accurate, since a molecule is by definition uncharged (or only partially charged).

@BillWilson — I look forward to your next publication in which you refer repeatedly to DNA as a complex of two polyatomic ions. The ion thing is irrelevant anyway (it is always balanced by cations) and you have essentially the same problem with haemoglobin. How are you going to refer to that? I think you need to emerge from your chemist’s cocoon and think about the state of science when, and the purpose for which, the term “molecule” was devised. Compare that with the state and purpose today, and the practicality of using words to communicate ideas.

@Bill Wilson The word "molecule" is usually meant to describe a "thing" on the atomic scale. Even the IUPAC definition essentially says a molecule is an "entity" bigger than 1 atom (note the lack of bond types). https://goldbook.iupac.org/html/M/M04002.html.     The reason why dsDNA is called a molecule is likely because the two strands behave as one entity in physiological contexts.

For all intents an purposes dsDNA "entities" will behave as a single molecule when handled in the lab unless you heat them above melting temperature or add chemicals and reactants that modify the strands.


text:
Estimating diffusion constant of a protein based on number of amino acids
Is there a way to estimate the diffusion constant of a protein based on the number of amino acids it is comprised of. I know that the shape of the protein has an influence on the diffusion constant, but I didn't know if there was some estimate that could still be used to good approximation.
If this does not exist, is there still a way to approximate the diffusion constant of certain proteins. I am trying to make a rough model based on reaction-diffusion equations, and I wanted to estimate diffusion constants of certain species in the model.

Also, you can check PDB if the structure of the protein is available. If so you can get a reasonably close estimate of its shape in vivo. If not, then you can check out some software that predict protein structure based on homologous proteins. However, I cannot say that there is a good estimate of protein diffusivity just based on number of amino acids. Are you interested in a particular protein or you want to make a general model?

@WYSIWYG After further reading it looks like I am looking at a cytokine that only has about 25 amino acids (49.5 kDa). I am assuming this might be easier to estimate a diffusion constant for since it is so small?

@AaronStevens someone could have measured diffusivity of cytokines in blood and ECF (for e.g.). If not, you can find the structure of a cytokine on PDB, obtain it's radius and estimate diffusivity using the Stokes-Einstein equation.


text:
Is there a way to determine corresponding differential equations from fitted Hill equation parameters
I am currently doing some work with GCaMP, a genetically encoded calcium indicator. According to the literature the Hill equation parameters for GCaMP6m is $K_d=167\pm3\, \text{nM}$ and $n=2.96\pm0.04$. Usually the "derivation" of the Hill equation assumes that a number of binding sites equal to the the Hill coefficient, but I understand that the Hill Coefficient should be interpreted more as an effective "interaction coefficient" rather than an actual indicator of how many calcium binding sites GCaMP6m has. This is certainly true here, since GCaMP is a fusion of GFP and Calmodulin, which has 4 calcium binding sites.
However, given that $K_d=167\pm3\, \text{nM}$ and $n=2.96\pm0.04$, is there a way we can formulate a set of differential equations describing the kinetics of calcium binding to GCaMP? Both "intuitive" ways I can think of don't seem to be valid. If we take the naive approach similar to the Hill equation "derivation" we would end up with equations like
$$\frac{\text dc}{\text dt}=-k_\text{on}c^n(g_T-g_c)+k_\text{off}g_c$$
$$\frac{\text dg_c}{\text dt}=k_\text{on}c^n(g_T-g_c)+k_\text{off}g_c$$
Now, $n=4$ is invalid because this would not produce the correct equilibrium behavior determined experimentally. However, $n=2.96$ would also appear to be invalid, as it doesn't correctly give the actual number of calcium ions taken up per GCaMP molecule.
Therefore, my question is how can we set up a correct (or reasonably correct) set of differential equations for a reaction given experimentally determined $K_d$ and $n$ that are more of "effective" parameters rather than literal ones?

@com.prehensible I am not asking a genetics question. Did I say something to make you think so?

I study digital signal processing, I'd have that in code for a graphical illustration. I can't figure out if the 6m version is very different from the GCaMP.


text:
Why did T cells have evolved to recognise self cells along with foreign antigent to generate a response?
T cells have evolved to be strain specific. For a T cell to respond it has to identify not only the foreign antigen but the antigen must also be attached to a self cell. what is the significance of that? Isn't that the reason behind autoimmunity and hypersensitivity? I understand about foreign antigen, but why self cells? the experiment by Zinkernagel and Dorothy about MHC restriction shows that same antigen presented by a foreign cell will not be killed by sensitized T cells.

Your question is unclear. "For a T cell to respond it has to identify not only the foreign antigen but the antigen must also be attached to a self cell", not really. The antigens have to be presented to the T-cell via the MHC. Can you please clarify?

yes, the antigen is presented by APCs via MHC, but there's a condition to that, the said APC must be a SELF cell, and T cells have to identify that the antigen is presented via a self cell only, otherwise there will be no reaction or killing or response. i mentioned an experiment in mouse by Zinkernagel and Dorothy. i am confused why cant a T cell simply kill the foreign antigen presented on the TCR  via MHC, why must it also be on a self cell. recognition of self cells is one of the causes of autoimmune diseases, so why did T cells evolve to be that way?

So please [edit] your question to clarify this. Comments are easy to miss and are not searchable. Also, add a link to the research you mentioned.


text:
Is there a Zipf law in epidemiology?
Are there cases where Zipf Law appears in epidemiology?
I ranked provinces of China by their coronavirus confirmed cases (2020-01-30 14:29):

4586, 428, 311, 278, 277, 200, 165, 162, 145, 142, 129, 114, 101, 101, 78, 70, 65, 63
  ...

Then I tried fitting the Zipf Law to it. I managed to get a good fit for a segment of it by using $x_n = 1600/n$:

4586, 428, 311, 278, 277, 200, 165, 162, 145, 142, 129, 114, 101, 101, 78, 70, 65, 63 ...
1600, 800, 533, 400, 320, 266, 229, 200, 178, 160, 146, 133, 123, 114, 107, 100, 94, 89 ...

The fit isn't very good, but good enough to be interesting. It makes me think there might be situations in infectious diseases where a Zipf Law appears. And by (Cristelli et al, 2012), I expect this situation to be particularly likely in places with a lot of economic and social integration.
I searched on Google Scholar with phrases like "Zipf infectious disease", but did not get anything interesting.

I am now aware of Zipf Law and its applications in biology but I want to ask what exactly are you trying to model? There are some well know modelling approaches for epidemiological data.

@WYSIWYG I'm just trying to figure out if Zipf's Law applies to this dataset. What it actually models, I'm not sure, but Zipf's Law applies to many phenomena for unknown reasons, so I think it'd be cool to see if it applies to epidemiological data.


text:
Sansevieria falling back to the wild form via leaf cuttings but not via micropropagation
I have heard that when you propagate Sansevieria via leaf cuttings, you get the wild form again. But if you use only meristem tissue, you can propagate the multicolored cultivated forms. What would be a possible explanation for this phenomenon?

This might be a better fit for [gardening.se].

A source for the claim would be a big help.


text:
mRNA vaccine and cell mitosis
What happens with the injected mRNA when cells are in the different stages of the mitosis process? Does the mRNA enter the cell and behaves normally throughout the mitosis phases?

I'd be interested in some reference. What made you think about the relationship of  m-RNA and cell cycle? (This reminds of some current issue: activation of LINE1 (LINE-1) retrotranscriptase, i.e. transcription of viral mRNA to DNA, depending on cell dividing or not).

According to this paper written by Abishek Wadhwa and his colleagues,  the vaccine mRNA will exert its function independent on active cell division because it is not integrated into the host genome [1].
Interestingly, I also found this paper which indicates that there is a possibility that the mRNA can enter the nucleus during cell division. During the prophase of mitosis, the nuclear membrane is dissolved, allowing mRNA to passively diffuse into and be included within the nucleus later during telophase. In addition, if endogenous reverse transcriptase is present, the mRNA can end up being integrated into the host genome [2].
Resources:

Wadhwa A, Aljabbari A, Lokras A, Foged C, Thakur A. Opportunities and Challenges in the Delivery of mRNA-based Vaccines. Pharmaceutics. 2020;12(2):102. Published 2020 Jan 28. doi:10.3390/pharmaceutics12020102

Sousa A, José M.M., Velilla A. Z.mRNA, Nanolipid Particles and PEG: A Triad Never Used in Clinical Vaccines is Going to Be Tested on Hundreds of Millions of People. Biomedical. 2021;34(1):2574. Published 2021 Feb 22. doi:10.26717/BJSTR.2021.34.005501

Please note that the first of these articles was accepted nine days after submission. This suggests it was not properly reviewed. In addition, the publisher of "Pharmaceutics" is "MDPI" — a publisher with a history of poor behavior and minimal peer-review. I would tend to treat articles published in such journals as highly suspect.

Predatory journals are a huge problem — you can learn more and see lists of predatory journals including the original Beall's List.

The second article, by Sousa et al., was published in the "Biomedical Journal of Scientific & Technical Research" which is not peer reviewed and seems to accept any paper if the fees are paid.  Among the gems it has published are "The Expression of the Proper-Name Effect Reinforces the Disarticulation ofCommunicative Rationality" and "Nietzsche and the Big Health. The Art as Culture’s Therapy".

@mgkrebbs I can't even hazard a guess at the content of the second paper.

@tyersome The 1st article was accepted about a month after submission (Received 2019 Dec 28; Accepted 2020 Jan 26), and it's a review. The timing does not seem to be an issue, although the publisher certainly may be.

@Armand — Interesting, I may of screwed that up, but I wonder if they've changed that info (nine days doesn't fit any of the currently listed publication related intervals) . At any rate this is a suspect journal and is being used to support an answer that makes dubious claims.


text:
Which cells do mRNA vaccines target?
mRNA vaccines instruct cells to produce spike protein that will trigger an immune response. But which types of cells will it work on? and which cells will it not work on?

I’m assuming the question refers to the Pfizer/BioNTech and Moderna vaccines in which Lipid NanoParticles (LNP) are used and to the injection to be intramuscular (i.m.). According to a blog by Derek Lowe [1], the parts of your body producing the coronavirus Sprike protein antigen are:

the muscle tissue at the site of injection, the lymphatic tissue downstream in your armpit on that side, your spleen, and (for the first day or two) your liver.

In other words, it is not only your muscle cells that become the antigen factory.

[1] Lowe, Derek (2021) “mRNA Vaccines: What happens”, Science Translational Medicine, AAAS, https://blogs.sciencemag.org/pipeline/archives/2021/01/21/mrna-vaccines-what-happens .

You might make it clear that the liponanoparticles do not contain any components that target specific cells. The site of injection and the propensity of cells to take up liposomes are the only factors involved. It would seem that the latter point is most relevant to the question. Do cells differ in this respect?

According to this paper written by Emily Bettini and Michela Locci, mRNA-LNPs and locally produced antigens are taken up by dendritic cells via endocytosis [1]. Within the cell, mRNA is translated into the antigenic protein. These locally produced antigens are either degraded by proteasome in the cytoplasm or secreted from the host cell, leading to 2 different immune response activation pathways [2].
When antigenic proteins undergone degradation by proteasome, the generated antigenic peptide epitopes are loaded onto MHC class I molecules within the endoplasm reticulum, then transported to and expressed at the plasma membrane [2]. When dendritic cells transfer to the lymph nodes, these loaded MHC class I peptide epitope complexes are recognized by CD8+ T cells. This pathway induces the formation of cytotoxic T cells which are capable of directly killing the infected cells [1].

Figure 1. Immune responses elicited by SARS-CoV-2 mRNA vaccines [1]
When antigenic proteins are secreted from the host cell, they are recognized and taken up by dendritic cells again. They are then degraded in endosome, loaded onto MHC class II molecules, followed by expression at the cell surface [2]. At the lymph nodes, these loaded MHC class II peptide epitope complexes are recognized by CD4+ T cells. This pathway induces the formation of memory B cells (MBCs) and the antibody-secreting long-lived plasma cells (LLPCs) [1].
Resources
1)Bettini E, Locci M. SARS-CoV-2 mRNA Vaccines: Immunological Mechanism and Beyond. Vaccines (Basel). 2021;9(2):147. Published 2021 Feb 12. doi:10.3390/vaccines9020147
2)Wadhwa A, Aljabbari A, Lokras A, Foged C, Thakur A. Opportunities and Challenges in the Delivery of mRNA-Based Vaccines. Pharmaceutics. 2020; 12(2):102. https://doi.org/10.3390/pharmaceutics12020102

"and locally produced antigens are taken up by dendritic cells via"  That's how the immune system processes them, but are those the only cells that take them up?  Or they are taken up by every other cell, too?

This is highly speculative, I don't think we know yet for CoV2 mRNA vaccines which cells produce the most spikes, the most MHC-I and where most (dendritic cells) MHC-II come from. The spike is not quite secreted, it is anchored onto the membrane.


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How are mRNA vaccines spread across the body?
Covid mRNA vaccines are injected into the deltoid. What is the process in which they spread from there to the rest of the body? Would there be a better immunization reaction if the second dose is injected elsewhere?

Why do you think the vaccine would need to spread to the rest of the body?

Mostly because of reports from Israel, US army and UK on miocardatis which may be linked to the vaccine in younger patients (although in the UK it is in low numbers compared with the others, but the age of the patients is older). If it is related, I'm trying to ascertain whether it could be from the mRNA instructions

https://meta.stackexchange.com/questions/66377/what-is-the-xy-problem

@KyuriOseetea The vaccine doesn't spread; instead, the immune system spreads its responsive elements.

https://www.docdroid.net/xq0Z8B0/pfizer-report-japanese-government-pdf#page=16
Pfizer's study for the Japanese government, cp. 2.6.5.5B. PHARMACOKINETICS: ORGAN DISTRIBUTION e.g. ovaries 23, testis 0,3 after 48 h.

The short answer to how vaccines are spread around the body is, quickly.

What is the process in which they spread from there to the rest of the body?

The reason vaccines are often delivered into muscle tissue is because muscle tissue is highly vascularized with both blood and lymphatic vessels. Immediately after a vaccine injection, the delivery vehicle (probably lipid nanoparticles or a viral vector) will quickly start diffusing into the blood, where it will be carried up to the heart, and from there begin spreading around the body (a lot of it ends up in the liver). Somewhat less quickly, in the lymph it will essentially start to generate an immune response immediately as it drains into lymph nodes and begins circulating throughout the lymphatic system (note the the desired immune response won't start until the genetic component of a vaccine has entered nucleated cells and has started being translated into the desired viral antigens).

Would there be a better immunization reaction if the second dose is injected elsewhere?

Don't know if I can definitively justify saying "no" to this question, but probably not. Muscle tissue seems to be the best injection site for vaccines. Deltoids are probably the best muscle because there's a lower chance of missing the intended injection site compared with some other muscles (e.g. glutes). And the systemic spread of vaccine components starts happening pretty fast after injection. In one animal study, researchers surgically removed a leg muscle 1 to 10 minutes after injection and still didn't prevent the related antibody response, or even really reduce it compared to animals with the muscle left intact.
Assorted References:
mRNA Vaccines: What Happens
Inadvertent subcutaneous injection of COVID-19 vaccine
The importance of injecting vaccines into muscle
Different patients need different needle sizes
Unmodified mRNA in LNPs constitutes a competitive technology for prophylactic vaccines
Differential dependence on target site tissue for gene gun and intramuscular DNA immunizations (1997)


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Herbivore digestive System
Why do Herbivores have many different types of digestive Systems? for example a Rabbit has a mono-gastric Digestive system and a hippopotamus has a pseudo ruminant digestive system but they are both Herbivores.

Rabbits and hippos are separated by ~95 Mya of evolutionary time: http://www.timetree.org/

This is kind of like asking why animals have so many different ways of moving quickly (dogs run, birds fly, kangaroos jump...)  There is a problem, and evolution has solved the problem in different ways.
In the case of herbivores (and in particular leaf and grass-eating herbivores) the problem is that their food is low in nutrients and high in indigestible cellulose. The particular solution depends on other evolutionary pressures.  For many leaf-and-grass eaters the solution is to become big, with complex many-chambered digestive systems that allow for long slow processing of the food. Horses, hippos and ruminants all tend to be large. This means that the animal can eat a lot and hold the food in themselves for a long time, allowing enzymes and gut bacteria time to work.
Rabbits, as burrowing creatures, can't evolve a large size, so depend on a range of gut bacteria and coprophagia to pass food through their intestines twice.
Grasshoppers can produce their own cellulase to break down cellulose without microbial assistance.
There's more than one way to do it and as a rule, in evolution, for every possible solution, some animal will be using it.

there are plenty of other factors as well, like grazers having to deal with highly abrasive food that browsers don't have to deal with.

Another factor is that there's not a strict divide between herbivores, omnivores, and carnivores.  Examples of each can be found on many branches of the mammalian evolutionary tree, implying that digestive systems must have undergone frequent modification.

"for every possible solution, some animal will be using it." is inaccurate - evolution has to discover a possible solution, and nothing guarantees that it will discover them all in finite time.


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What Old World fish produces "white gems" in its brain?
In his ancient list of "white gems," Isidore of Seville mentions the "cinaedia," which he describes as follows:

Cinaedia is found in the brain of a fish with the same name; it is
white and oblong. People say that with it they predict calm or storm
at sea (Etymologies 16.10.8)

This seems to match the description of a lucky stone, except that freshwater drums (Aplodinotus grunniens) would hardly have been endemic to Isidore's (Old World) setting. What fish could Isidore have been referring to?

Otoliths are common (if not ubiquitous) among fish. I think the solution is to figure out what fish would have been called Cinaedia, which isn't so much a biology question as a Spanish language or etymology question.

@kmm It would be a Latin question, not Spanish but I think you're right and this is not really on topic. I posted an answer since I did find a reference, but I'll also vote to close.

I’m voting to close this question as off topic because it isn't really about Biology but about what a specific Latin name for a fish meant.

Turns out there's a paper that has looked into this:  Christopher John Duffin (2007). Fish Otoliths and Folklore: A Survey. Folklore, 118(1), 78–90.         doi:10.2307/30035398. The paper investigates the history and folklore associated with fish otoliths, and includes the following note:

Claudius Aelianus (On the Characteristics of Animals IX. 7; see Aelian 1959) (c. 175-235) suggested that
"Cinaedius" might be the Bass, and thus synonymous with Lupus.

So, based on my (very) cursory reading of the paper, it looks like it isn't entirely clear what fish was referred to by the name Cinaedius in Latin, but Bass is a contender.

Seems that leaves the question "which bass", especially given the diversity of species that carry that label, though at least it's more narrow than "fish".


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Is it possible to kill parasitic worms by intoxicating oneself?
I've heard of parasites that can live in the human body and do a lot of damage to the host. There are even safer forms of worm-like parasites inside the intestine, but some parasites can live in the blood vessels or even in the brain or eyes.
Parasites are, in my opinion, the most disgusting creatures there are, so I wondered if they could be killed with intoxication.
Would it be possible to get rid of worm parasites in the blood by increasing the amount of alcohol in the blood to a level that humans can tolerate but parasites can't?
Could you also eliminate brain parasites with hangover-related brain dehydration?
That the dead parasites remain in the body may not be good or advisable. In addition, eggs, which are usually a little more resilient, should rather be removed from the body by antibiotics or proper medication. But is it at least theoretically possible to do something with alcohol against parasites?

In summary, there is no convincing evidence to say that alcohol intoxication helps to treat or prevent parasites in humans.
1) The evidence from in vivo human studies does not support the idea that alcohol consumption helps in treating parasites.
Alcoholism and Strongyloides stercoralis: Daily Ethanol Ingestion Has a Positive Correlation with the Frequency of Strongyloides Larvae in the Stools (PLoS, 2010):

The frequency of Strongyloides was significantly higher in alcoholic
  patients than in control group (overall prevalence in alcoholic 20.5%
  versus 4.4% in control group; p = 0.001).

2) Even a strong alcohol beverage gets diluted when it reaches the intestine.
Ethanol concentrations in the human gastrointestinal tract after intake of alcoholic beverages (European Journal of Pharmaceutical Sciences, 2016):

In a cross-over study, five fasting volunteers were asked to drink two
  standard consumptions of commercially available alcoholic beverages,
  including beer (Stella Artois®, 500 mL, 5.2% ethanol), wine (Blanc du
  Blanc®, 200 mL, 11% ethanol) and whisky (Gallantry Whisky®, 80 mL, 40%
  ethanol).
The median gastric ethanol Cmax (min–max) for the beer, wine and
  whisky conditions amounts to 4.1% (3.1–4.1), 4.1% (2.6–7.3) and 11.4%
  (6.3–21.1), respectively...Median duodenal ethanol Cmax (min–max) for
  beer, wine and whisky are 1.97% (0.89–4.3), 2.39% (2.02–5.63) and
  5.94% (3.55–17.71), respectively.

So, the maximal ethanol concentration in the duodenum after drinking 80 mL of whisky was 17.7%. Most of ethanol is absorbed in the first part of the small intestine (Scandinavian Journal of Gastroenterology), so it does not reach the more distant parts and does not likely kill the parasites there.
3) Even strong intoxication is associated with low blood alcohol concentration.
In strong intoxication, your blood alcohol concentration would be only 0.2-0.3%. In one study (Table 1), the 50% lethal concentration (LC50) of ethanol, which killed 50% of the bloodstream forms of the parasites Trypanosoma brucei, was 10.6%.
4) Alcohol intoxication and brain dehydration
Alcohol intoxication or hangover are not automatically associated with dehydration. Anyway, even in severe dehydration, you still have a lot of water in your body, including the brain, so the parasites living there do not necessarily get dehydrated as a result of your dehydration.
In general, dehydration increases the risk of infections, because it dries mucous membranes, for example in the urinary tract (BMJ Open Quality, 2019).

I don't think I'll ever drink alcohol again. No, but seriously, parasites are really creepy. It's good to know that I can't do anything against parasites with alcohol and would even have a higher risk of infection. So thank you for the good answer.

@user1136, the OP asked if alcohol can kill parasites. I have found that single in vivo human study, which does not support this idea. No matter how weak or poorly related this evidence is, it does not suggest that alcohol can help. Chronic alcoholism is a series of severe acute alcohol intoxications, anyway. That same study also does not support the idea that alcohol would repel parasites or make them less productive as in the fruit-fly and wasps study. I mean, it could - but where is the evidence?

This is a great well-cited answer. Just to add one more thing to discourage getting drunk to treat the parasite; a viable treatment is assessed via the risk-benefit ratio. Even if these studies were not present, becoming highly intoxicated may do as much damage to the host as the parasite you are trying to eradicate. According to the NHS, there is no safe level of alcohol consumption.

@user1136 You raise an important point that the PLOS study is limited in scope. And re the wasps, there is no doubt external use of alcohol can kill pathogens. This question addresses evidence surrounding ingested alcohol and if there are any associations with parasitic resistance or treatment.

Although the previous answers give a resounding "No" for the case of human hosts and parasitic worms, a 2012 research paper (Alcohol Consumption As Self-Medication Against Blood-Borne Parasites In The Fruitfly) states that the larvae of Drosophila melanogaster (fruit flies) actively seek out foods containing ethanol when they are infected by the eggs/larvae of parasitic wasps.
(I don't know whether they do this when the parasite's egg has been laid inside them, or after it's hatched into a larva, or both.)
This paper was quoted by various popular science magazines of the time (see e.g. https://www.newscientist.com/article/dn21493-parasite-plagued-flies-self-medicate-on-booze/), and also metioned the use of ethanol as a preventative measure as well as a curative one.
Despite having evolved an increaed tolerance to the ethanol, however, the increased consumption may have some adverse side-effects on the infected fly larva.

Generalising from alcohol to toxic substances in general - caterpillars of the Grammia incorrupta moth consume plants containing toxic pyrrolizidine alkaloids (PAs) to kill the eggs of parasitoids within them. The PAs are poisonous to the caterpillar as well as the parasites, and caterpillars that successfully exploit this strategy still suffer adverse health effects. https://web.archive.org/web/20160313220351/http://phenomena.nationalgeographic.com/2009/03/20/self-medicating-caterpillars-use-toxic-plants-to-kill-parasites/

The New Scientist article you linked does not mention any use of alcohol for treatment of worms or other parasites in humans.

The answer to your question depends on the kind of parasites you're focusing on.
Looking at bacteria and gastro-intestinal infections, I found three articles (one based on a model stomach, a second one based on a questionnaire and serum analysis and a third one describing a specific incident), which indicate that there is a certain protective effect of ethanol consumption.

This paper describes the effect of wine on Listeria innocua in a model stomach (I have only access to the abstract). Wine seems to have an antimicrobial effect, which can be traced back mainly to ethanol as well as to organic acids.

Ethanol exhibited a higher bactericidal effect than the mixture of the main wine organic acids. When testing the organic acids separately, malic and lactic acids were found to have the strongest effect. The combination of ethanol with the organic acids acted synergistically but to a lesser extent than wine itself.

If anyone has full access to this article it would be interesting to put it into perspective to point two of the (currently) accepted answer.

This paper, based on a questionnaire on dietary habits and serum analyses for for Helicobacter pylori immunoglobulin G antibodies (1'785 participants), comes to the conclusion that

[t]here was a clear inverse dose-response-relation between reported alcohol consumption and H. pylori infection.

[Also here, only the abstract is accessible.]

There is another paper describing the effect of alcohol consumption on a Salmonella outbreak in Spain. The sample size is relatively small (90 people), but the data suggests that

[t]here was a protective effect of alcohol that was stronger among the people who drank more than 40 gm of alcohol.

Welcome to Biology.SE! Nice answer and a good job on providing supporting references. However, can you please include the complete reference information since links can break. Search on Google Scholar and click on the ‟ symbol to get reference information for journal articles. This is a good example of how to format references. Thanks!

However, please note that the original question was about worms rather that bacteria. If you can't find a question for which this is a relevant answer on this site (I gave a quick look and didn't find any), I would suggest posting a relevant question and then move this answer to that question.

From the first principles:
The most sensitive to alcohol part of the human body is it's nervous system. Worms have much simpler (in both biochemistry and organization) nervous system, so they will probably suffer less from a generic poison that the alcohol is.
OTOH, you can easily find a substance that is WAY more toxic to the worms than to yourself. Up to and including being safe to be given to minors and reproducibly killing all the worms. Just ask the nearest pharmaceut.
p.s. in the same sense, alcohol is killing bacteries, but you cannot cure pneumonia by drinking, no matter what heavy drinkers assert.

+1 The key is finding something worse for parasites than for humans. Alcohol isn't likely to be the best candidate, and there is a whole sector of pharmaceutical industry devoted to optimising and producing alternative substances.


text:
What does basipetal succession (of flowers/leaves) mean?
The definition says that basipetal succession is the arrangement of flowers such that the older ones are present at upper side and the young flowers are arranged towards base. But in this diagram:

the oldest flower is at the base and the youngest is towards the upper side. Can anyone help me understand this?

The definition you quote is a bit misleading — what matters is where the lateral flowers are connected to the inflorescence axis, not where they are physically in space.
Thus, due to the way these cymes develop (starts with a terminal flower and then a lateral bud grows out to form anther terminal flower, etc.) they must be basipetal because the first flower to develop is the terminal flower.  In other words, for cymes the lateral buds tend to overgrow so it looks like they are above, but what really counts is where they are placed on the inflorescence axis (which is below).
You may find this explanation clearer than the one in your textbook.

In my book, it says that Helicoid and Scorpiod Cyme are examples of Cymose Inflorescence which shows basipetal succession of flowers.

Sorry, my original answer wasn't very good — I hope the edited version is more useful to you!

Thank you, I really understand this much better!

You're very welcome!


text:
What would the ploidy of a multinucleate cell be?
If we have a haploid organism, and it undergoes karyokinesis without cytokinesis, would the organism be considered haploid or diploid?

Ploidy is generally defined in terms of the number of chromosomes in the nucleus, rather than the number of chromosomes in the cell.
Some examples in support of this:
- A paramecium has a diploid micronucleus and polyploid macronucleus
- Muscle cells are generally considered diploid even though they have multiple nuclei
- The additional chromosomes in mitochondria and chloroplasts are not considered to make cells polyploid, even if the organelle itself may be polyploid.
Thus, I would assess a cell such as you describe to be haploid, albeit with two nuclei.

This was very helpful, thank you so much!


text:
Meaning of units in ELISA based tests?
For some ELISA based antibody tests (e.g. h-tTg antibody test), labs report units as RU/mL or U/mL. Also different labs have different cut off (normal range) values.
I understand that different kit manufacturers recommend different ranges because the units are not standardized (e.g. IU/mL) for enzyme activity concerned. But I didn't understand the difference between RU, U and AU
Question
Is there a difference between RU/mL, AU/mL and U/mL? Are the figures comparable across reports from different labs (which may be using different kits)?

No actually. U is definitely not IU. I am referring to ELISA tests where there is no international standards yet. For example, IgA tTg antibody test. I know AU is Arbitrary Units. RU is either Relative or Reference Unit. U is simply unit. Doubts is what's the difference between these.

Thanks for informative comment. I am not from biology background so your comment helped. Now what I meant by standardization is that what conjugate to use and incubation times are not standardized for some tests. Because of this, extinction coefficients are not known. So the lab depends on calibrators given in the kit. Calibrators have specified units and using that curve is fitted. Based on fitted curve sample's concentration is derived. Now, from what i read, manufacturers give their own units. But some give RU some U some AU. For tests where standard reaction conditions are defined IU.

The ELISA kits are calibrated to meet the requirements of
  internationally certified laboratories such as Center for Biologics
  Evaluation and Research (CBER) associated with FDA. In most cases, the
  presence and specific concentration of an antigen is the target for
  the measurements. Such measurements take place through the absorbance
  measurement. According to the Beer-Lambert law, concentration of a
  compound in a solution is proportional to the quantity of light
  absorbed at its specific wavelength and at a constant optical
  path-length. Following absorbance measurement, a simple calculation
  leads to the concentration of the analyte via equation below:
A = εlc
where A is absorbance of the solution at the particular wavelength, ε
  is the molar absorptivity, l is the path length or deepness of the
  solution (which for common spectrophotometers is 1 cm or less if a
  well plate reader is employed), and c is the concentration of the
  substrate in the reaction solution (M or mol/dm3). Majority
  of ELISA microplate readers correspond to this method for the
  calculation of the analyte concentration. Introducing standard
  solutions with known analyte concentrations can be the basis of such
  calculations for the instrument. Measurement unit are typically
  expressed in gram per liter (g/l), mol per liter (mol/l) and copies
  per milliliter (copies/ml) for nucleotides, plaque forming units per
  milliliter (pfu/ml) for infectious viruses, colony forming units per
  milliliter (cfu/ml) for cells and phages, as well as unit per
  milliliter (u/ml) for specific enzymes. These measurement units can be
  also reported over time (i.e. ng/ml/h). Relative units (RU/ml) or
  equivalent units (Eq/ml) are normally used if no international
  standard references exist for the conversion.

Source: Enzyme-linked Immunosorbent Assay (ELISA): From A to Z (SpringerBriefs in Applied Sciences and Technology) by Samira Hosseini, Patricia Vázquez-Villegas, et al. | Dec 31, 2017; ISBN-13: 978-9811067655; ISBN-10: 9811067651. Page 65.
Contrary, Units Per Millilitre (U/mL) are normally used when there are international standard references, agreed upon by scientists and doctors.
Please find the following information on Arbitrary Units (AU):

The WHO Expert Committee on Biological Standardization (ECBS) is the
  scientific body that establishes WHO biological reference standards
  which serve to define an internationally agreed unit to allow
  comparison of biological measurements worldwide. WHO International
  Standards (IS) for biological substances are recognized as the highest
  order of reference materials for biological substances and they are
  assigned potencies in International Units (IU). International
  Standards are used to quantify the amount of biological activity
  present in a sample in terms of the IU, allowing comparisons between
  assays from different laboratories.  Calibration of assays using
  System of Units (SI)units is not appropriate given the variability of
  the specific activity of a biological material. Use of an arbitrary
  unit makes it possible to better define parameters such as the
  analytical sensitivity of tests or clinical parameters such as
  protective levels of antibody.

Usually, arbitrary units are defined within a particular study. For example:

A human serum pool positive for anti-dsDNA IgG antibodies (DNAPo) was
  prepared by mixing equal parts of serum from 10 patients with SLE who
  had a positive CLIFT test ≥ 1:640. The DNAPo was arbitrarily designed
  as having 100 arbitrary antibody units (AU) per ml. Artificial serum
  standards containing different AU/ml were prepared by diluting the
  DNAPo with phosphate-buffered saline (PBS) containing 0.1% Tween 20
  (PBS-T). A human serum pool negative for anti-dsDNA IgG antibodies
  (DNANe) was prepared by mixing equal parts of serum from 10 healthy
  persons who had a negative CLIFT test and no clinical evidence of SLE.
  The DNAPo and DNANe pools were used as positive and negative controls
  in the ELISA and CLIFT reactions.

Thus, the U/mL figures are comparable, while RU/ml or AU/ml are not.

Thanks for the answer. I thought when there are international standard references, IU/mL is used. In any case what does AU mean?

@Dayne, thank you! I have updated my answer on AU (arbitrary units).


text:
Nonlinear (Quadratic) selection gradients formula
Under scenarios of stabilizing or disruptive selection, we can add a quadratic component to our model of phenotype and fitness like so.

Specifically, I am not clear on where the 1/2 comes from nor do I understand the derivation of gamma, which is equal to as follows:

x is the phenotype of interest, w(x) is the fitness of said phenotypic value. uBS is the mean phenotype before selection. Any help would be greatly appreciated.

Hi, do you have a link to where those equations are from? Thanks.

Those two equations come from Lande and Arnold 1983 per the comment below this one :) Sorry!

Coefficient $1/2$ is a matter of definition/convenience. One could have written $\beta x_i + \gamma x_i^2+\bar{w}$, but then a factor of $2$ would surface in the other forumals.
The other two equations are adapted to one-dimensional case (one trait) from the Lande and Arnold's paper The measurement fo selection on correlated characters. In particular, the equation with covariance is their equation (13a), which follows from their more general equation (4) for quadratic selection. The last equation is the restatement of their (14b).
Update
Here I retake the notation of the above-mentioned article by Lande, but adopt it to the case of a single trait. Then the variance matrix $P$ is just a number (variance). Equations (14a) and (13b) define
$$\gamma=\frac{1}{P^2}C, (A)\\
C=Cov\left[w, (z-\bar{z})^2\right],
$$
which is the definition of $\gamma$ in the OP. It is essential here to use the correct expression for the covariance:
$$
Cov\left[f(z), g(z)\right] = \int \left[f(z)-\bar{f}\right]\left[g(z)-\bar{g}\right]p(z)dz=
\int f(z)g(z)p(z)dz -\bar{f}\bar{g}
$$
In our case we thus have:
$$
C = \int w(z)(z-\bar{z})^2p(z)dz - \bar{w}\overline{(z-\bar{z})^2},
$$
where $\bar{w}=1$ by definition, whereas $\overline{(z-\bar{z})^2}=P$ is the variance of the trait. We thus have
$$
C = \int w(z)(z-\bar{z})^2p(z)dz - P, (B)
$$
where
$$
p(z)=\frac{1}{\sqrt{2\pi P}}e^{-\frac{(z-\bar{z})^2}{2P}}.
$$
Let us now consider the integral
$$
\int \frac{\partial^2w(z)}{\partial z^2}p(z)dz=
\frac{\partial w(z)}{\partial z}p(z)|_{-\infty}^{+\infty} - \int \frac{\partial w(z)}{\partial z }\frac{\partial p(z)}{\partial z }dz=\\
\frac{\partial w(z)}{\partial z}p(z)|_{-\infty}^{+\infty} -
w(z)\frac{\partial p(z)}{\partial z }|_{-\infty}^{+\infty}+
\int w(z)\frac{\partial^2 p(z)}{\partial z^2 }dz
$$
The first two terms vanish, since $w(z)$ is bounded, whereas $p(z)\rightarrow 0$ as $z\rightarrow \pm \infty$.
We thus have
$$
\int \frac{\partial^2w(z)}{\partial z^2}p(z)dz=
\int w(z)\frac{\partial^2 p(z)}{\partial z^2 }dz=
\int w(z)\frac{\partial^2 }{\partial z^2 }\frac{1}{\sqrt{2\pi P}}e^{-\frac{(z-\bar{z})^2}{2P}}dz=\\
\int w(z)\left[\frac{(z-\bar{z})^2}{P^2}-\frac{1}{P}\right]\frac{1}{\sqrt{2\pi P}}e^{-\frac{(z-\bar{z})^2}{2P}}dz=
\int w(z)\left[\frac{(z-\bar{z})^2}{P^2}-\frac{1}{P}\right]p(z)dz=\\
\frac{1}{P^2}\int w(z)(z-\bar{z})^2p(z)dz - \frac{\bar{w}}{P}=\\
\frac{1}{P^2}\left[\int w(z)(z-\bar{z})^2p(z)dz - P\right]=\frac{C}{P^2}=\gamma,
$$
where we used $\bar{w}=1$, and equations (A) and (B) above.

The notation in the Lande and Arnold paper is incredibly difficult for me. If you look at 14b, could you help me understand the math that describes why the first part of 14b is equal-to the second part of 14b. I run a population genetics club and this will be incredibly helpful for us.

Essentially the same question as above in the sense that am confused about making the connection between the two equations for gamma above in this thread.

@user6817734 I have added the details of calculations. I hope it helps.

This is absolutely incredible. Thank you so very much.


text:
How can animals that rely on SONAR not see color?
Humans can sense colors with acuity and can distinguish them because of the light of different spectrum that follows into their eyes. Not its also said that sound is different for different colors,
Wouldn't this mean that during echolocation , dolphins, Bats and other animals can see colors? Please explain

"its also said that sound is different for different colors" - said where and by whom?

@Bryan Krause https://en.m.wikipedia.org/wiki/Colors_of_noise#:~:text=Different%20colors%20of%20noise%20have%20significantly%20different%20properties.&text=Other%20color%20names%2C%20such%20as,of%20light%20with%20similar%20spectra.

That article has nothing to do with visual color except a modest analogy. Also has little to no relationship to echolocation sounds. "Noise" in this context isn't even necessarily related to any sort of sound, but rather to random patterns which can be in any sort of signal.

@Bryan Krause  oof yeah you're right I should've read it better, sorry

I’m voting to close this question because it is unclear and seems to based on a fundamental misunderstanding of a non-biological concept (color).

Color is a characteristic of visible electromagnetic spectrum, see the graph here. Electromagnetic means here that it has the same nature as radio-waves, X-rays, and gamma radiation, whereas visible refers to the region of spectrum - waves of frequencies ranging from TeraHertz to PetaHerz (i.e., from $10^{12}$ Hz to $10^{15}$ Hz). Specific colors essentially refer to sub-ranges of the visible spectral range (ordered as in a rainbow).
On the other hand, sound waves, used in echolocation, are waves of material compression/decompression in air, liquid or solid, and their frequencies rarely exceed one MegaHertz (that is $10^6$ Hz, i.e., $10^6$ oscillations per second). E.g., human ears distingushes sounds in the range from $20$ Hz to $20$ kHz, whereas animal sonars use ultrasound frequencies above the human hearing threshold - from $60$ kHz to $200$ kHz (see here).
To summarize: sonar and sound have nothing to do with color perception.

The question is based on a false premise.  Humans (and other animals) perceive color because they have sensors - in the case of humans, three types of cones - that respond to different frequencies of light.  "Color" is really a construct of the brain, as it interprets the intensities of the signals from the different receptors.
Sonar is more analogous to the rod visual system, used in low-light conditions where you can see things, but not distinguish their colors.
Of course an animal echolocation system (or a technological one) could potentially distinguish something analogous to color, by having receptors that respond to different sound frequencies.  But the sound reflection characteristics of objects would have nothing to do with their colors.  That is, a hard red surface would reflect sound differently than a soft red one.

Bats at least seem to have fairly sophisticated sense of texture, probably the best analog for "color vision" in this context. https://www.pnas.org/content/101/15/5670 for example

@Bryan Krause: Interesting!  I learned something new :-)


text:
How fast do ions move in body when they go in and out of the cell membrane?
Do we have any measurement tools to measure the speed of ions moving in a human body, specifically going in and out of the cell membrane? Do we have any tools to know where an ion is at a specific time?

Why do you want to know? Might https://meta.stackexchange.com/q/66377/401068 apply to your question? See also https://en.wikipedia.org/wiki/Brownian_motion

We do - check out patch-clamping


text:
Where can I find the exact base pairs for a specific gene, e.g. SRY (sex determining region Y)?
Per a quora answer, the Sex-determining Region Y (SRY) gene contains 14 bp. I searched the gene on NIH and genenames and get just the info about the gene itself.
Where can I find those exact 14 base pairs for the gene?

First of all, the information on Quora is wrong: The SRY gene transcript is 828 nucleotides long and encodes for a protein of 204 amino acids. 14 base pairs would only code for 4 amino acids which is not really a functional protein.
You can download sequence information from Ensembl (or also the NCBI if you like, the datasets behind it are the same). Go to the Ensembl Website choose human and type in the gene you are looking for.
You will get back a page which looks like the following:

On the left side you can now either click on "exons" or "cDNA" to get a closer look on the sequence:

This is what you get when you choose cDNA. It shows the complete transcript in the first line, the processed, protein coding sequence in the middle and the protein sequence below each triplett. You also have a download button for the sequences, if you press it, you can decide which information you want to have (full transcript, mRNA...) and the format (simple text or annotated rtf file):

Choose the information you are looking for and then save it to your computer.


text:
What is the Definition of Homologous Chromosomes? length, gene position are the same or similar?
what is the Definition of Homologous Chromosomes?
this post says

Homologous chromosomes are chromosome pairs (one from each parent)
  that are similar in length, gene position, and centromere
  location.

and then

The position of the genes on each homologous chromosome is the same.

are length, gene position of a pair of chromosomes the same or similar?
if exactly the same (I guess not), job well done.
if just similar, What is the Definition of similar? 99% same?
in the case of a pair of human Chromosome 1, what is the exact number of base pairs that are the same?

Before posting to this site you should research your question. Although you have cited one source, there are better places to look. You need to understand the (molecular) biological concepts rather than make the mistake of physical scientists in thinking things are defined by numerical cutoffs. Wikipedia can be a good source, and here gives a good basic explanation, which is fleshed out in the section on meiosis in Alberts et al. on NCBI bookshelf — an excellent resource.

Unfortunately despite the impression given by the many poor explanations available (including the one you quoted), homologous is not a synonym for similar.
Homology is defined as the existence of shared ancestry1,2.  Thus, structures being homologous simply means they had a common ancestor — i.e. homology is a relationship not a property of an individual structure.
The "definition" you quote is actually a description of what you typically see when comparing two homologous chromosomes within a species. High levels of sequence similarity suggest homology, but are not sufficient to prove it.  (To test that requires building phylogenetic trees.)
(One classic example of this is the superficial similarity between dolphins and sharks, which is an example of convergence not homology.  Another is the homology between bird and bat wings — they are not homologous as wings, though they are homologous as tetrapod forelimbs.)
Consequently, for two chromosomes to be homologous they must have descended from a (potentially much earlier) chromosome that has been duplicated possibly for many generations (the ancestral chromosome might even have existed in a now extinct ancestral species).
So, if an inversion happens within a chromosome (and changes the ordering of the genetic loci) that chromosome is still homologous to the parental type chromosome that didn't undergo inversion.
ETA: Note that chromosomes don't need to be in the same cell (or even the same species) to be homologous and chromosomes can be homologous even if the cell they are in is not diploid.  For example, the human chromosome 1 is homologous to the chimpanzee chromosome 1.

Similarity is a measurement of "distance" between sequences, but while very similar sequences are likely to be homologous there is no magical value of similarity that proves (or disproves) homology.

Individual humans are about 99.9% identical (depends on how you measure this) at the nucleotide level, so that will also be true for chromosome 1.

Finally, the UC Berkeley Museum of Paleontology also has useful resources for understanding evolution including some material on homology — e.g.:
https://evolution.berkeley.edu/evolibrary/article/lines_04

References:
1: Brigandt, Ingo, "Essay: Homology". Embryo Project Encyclopedia (2011-11-23). ISSN: 1940-5030 http://embryo.asu.edu/handle/10776/1754.

2: Mindell, D. P., & Meyer, A. (2001). Homology evolving. Trends in Ecology & Evolution, 16(8), 434-440.

Sorry to be a wet blanket after all your work, but it seems to me this is not answering the (very naive) question which is about diploidy — at least the first quotation — the poster perhaps confusing it with the use of homology in relation to similar genes or gene regions (but seldom chromosomes) between species

The first link the poster gives has a classic picture of a pair of human chromosomes and refers to one being maternal and one paternal. It doesn’t say anything about diploidy, but that is what that reflects (isn’t it) and was a choice of words to try to explain what I thought was your misinterpretation. The term “homologous chromosomes” was (I imagine) used years before the term “homologous” was used in comparing the sequences of genes from different organisms. PS Criticize my arguments, say if you think I am violating the code of conduct, but please do not make general personal observations.

@David: My apologies, that was not intended as a personal attack. I will delete the offending comment and be more careful in the future to keep my focus on content. ——— I still don't see why you think the OP is asking about diploidy.  The concept of homologous chromosomes are most commonly introduced during discussions of meiosis (which in my experience will always be presented in a diploid context for lower level students). Consequently it seems natural to discuss the concept of homologous chromosomes in a diploid. However, I will edit my answer to emphasize this distinction.