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What causes people to smell one persistent smell during Covid-19 infection?
Some of the people I know got COVID and they lost their sense of smell. They told me that they perceive one persistent smell, everywhere (like onion). Is this frequent for people with loss of smell? How this is possible?

Does this answer your question? https://biology.stackexchange.com/questions/97914/loss-of-taste-and-smell-during-a-covid-infection

I already saw this but it'doesn't answer my question: I do know why people loss the smell but I want to knwo why for some people the smell of things is replaced by one particular smell

I could guess it's similar to tinnitus (which doctors still cannot explain well): You "hear" a tone that isn't there. Or even worse: You cannot hear the tone (e.g. 12kHz) that tinnitus makes you hear occasionally.

Note that there some "smells" that are not perceived through the olfactory system but through the trigeminal system, see, e.g., F. Viana, Chemosensory Properties of the Trigeminal System, ACS Chem Neurosci. 2011 Jan 19; 2(1): 38–50. The pungent smell of onions belongs, among some other chemical sensations, to this group.
Thus, when the olfactory system is blocked, there are still "smells" left and one perceives them more prominently than usual.

Very interesting ! Thank you for your answer !

At this time any hypothesis regarding the parosmia seems to be untested.  Speculative sentences in lay and technical sources point toward the olfactory bulb.  (I have seen indications regarding the cilia of the olfactory neurons, the bulb itself, and the blood supply, but this seems to stray from our topic)
When we look in more detail, the olfactory bulb consists largely of glomeruli (balls of neuropil about 0.1-0.2 mm in size), which receive input from specific kinds of olfactory neurons that receive from specific odorant receptors (ORs).  See this figure for the situation in mice.  The dorsal region of the olfactory bulb is mostly one type of these, Class I ORs, and the ventral part is all Class II. (more)  If you are following this research you might want to try to figure out if the odors people report are mostly Class I (more hydrophilic) or Class II (more hydrophobic), which might allow you to hypothesize something about the relative strengths of signals from these regions in the model you develop.  Reading anecdotes is scientifically useless, but fascinating - this man describes citrus as tasting "extremely oxidized", which certainly fuels a speculation along that line.
Answering the question in any good way would seem to demand good human olfactory tissue from people who catch Covid, suffer ongoing parosmia, die from something else, and then donate their brains to science.  I'm not sure we're going to see a definitive answer that way soon.  It would be worth keeping an eye out for fMRI data.  I suspect that well-focused high-frequency terahertz might be used to image or even stimulate olfactory glomeruli (phones with 'smell-o-vision') but for now that's science fiction.

France have a law that make you donate limb by default, so we better keep an eye on it !


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How are vaccines mass-produced?
I have a background in product design and so am familiar with with how most things are mass-produced — food, machines, etc.  But I've been able to find very little information on how vaccines are mass-produced.
It looks like there are 4 types of vaccines, all of which include pieces or byproducts of the virus they're intended to counteract.
If you're producing billions of vaccines, I imagine you need a tremendous amount of the virus.
How is such a mass of virus obtained? Do they just fill up tanks with a culturing agent and a sample of the virus and wait for it to grow, like a giant petri dish? Are there big vats of Coronavirus sitting in factories somewhere?

Did you read the part of the page you linked about the mRNA vaccines for covid-19?

I’m voting to close this question because it is about industrial pharmaceutical practice, not biology.

@David I would disagree with that assessment. This seems to me to be very much about "techniques in a biological ... laboratory" just for higher scale operations.  Or is this site intending to exclude all discussion of bio work beyond MRL 3?  Scale-up is a massively important part of biotech R&D.

@jakebeal — No. Industrial biotechnology is not laboratory biology, and the people who are able to answer questions on biology based on their biological education and research and teaching experience seldom know any more about it than an educated non-biologist with access to the Internet. And I emphasize that this is not a discussion site — it is a question and answer site. If the question is such that it is unlikely to attract objective expert answers on a SE site is should be neither asked nor answered there.

@David Your response assumes that experts from industry should not be interested in this site, not to mention experts from academia who interact with industry.

@jakebeal — "should not be interested in this site"? Not unless they have questions about problems in biology of the type this site was set up to answer. If you mean contribute answers, their historical lack of participation speaks for itself. But even if this question were on topic, it is so vague and its scope so wide that I regard it as unsuitable. There is a Help entry somewhere about answers that require a book chapter to answer.

@David I'm currently working with algae, scaling up and investigating mass production is a big part of the area and a follow up research we must do. This will give me enough information and experience to answer this kind of questions in the context of algae, so I think this question should stay open

@Hachiloni — "This will give me enough information…"? What do you mean by this. There is only one answer which in my opinion provides no information. You may well be interested in the question, but if it is on the wrong list it won't get any answers. Wishing that experts in this area visited this list to provide their expertise is unrealistic.

@David I mean that this kind of questions can be answered on this site, so closing this question will give a bad precedent. I gave an example how I could answer a question of this kind with my knowledge

@Hachiloni I'd like to invite you to commit to the proposed Synthetic Biology site, where questions like this will be clearly on-topic and welcomed: https://area51.stackexchange.com/proposals/125068/synthetic-biology?referrer=MjE2YzEyZjY2NGZiZjQyMmQxNjM4YzE1ZTgyMTBjM2M1ZThhODIyZjc0OGY4MjUwNjQzYWUyYjcxYzdjNjgyZWgojuPHgTg3aSlhs7HovzJGQ8mR63x7oTvvqF7pWvWl0

Per Wikipedia, typically when one needs a lot of virus, it is grown in a controlled cell environment. This used to be eggs, but is moving toward cell cultures instead.  So basically yes, factories full of virus (though more like in nice discrete bioreactors than big Joker-friendly vats).
Synthetic vaccines, such as the mRNA vaccines for COVID, do not need this step at all, since they do not actually use the virus, but can be done through cell-free biochemical reactions that replicate the mRNA directly.

I used to work in a flu vaccine manufacturing facility, and we would go through millions and millions of eggs each season, sourced from local farms. It was quite a sight to behold...

source: Stack Exchange

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

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The Perfect Predator?
I’m not a biology major or even studying it in any way so I apologize if this makes no sense.
I’m curious, if say the Jurassic Park team came up to you and asked you to genetically engineer the perfect predator, what characteristics would you give it?
And I guess by "perfect predator" I mean a predator that could consider any living thing prey? Sorry again if this doesn't make sense.
Besides the obvious “Super strength” or “Super speed” or things that make no sense at all like “laser eyes” of course.
I’m thinking things like a flexible spine that expands and contracts to increase its bound when it runs, like a cheetah or etc.
Feel free to include any features from extinct or even made up animals as long as its actually theoretically possible (again no laser eyes!!)
Like I said this is not for any research or anything, purely for my own curiosity so any thoughts are welcome. Thanks!

Biologically, the notion of a "perfect predator" isn't well-defined, because it isn't clear what is being perfected.
Predators are just organisms that eat other organisms. What would it mean to be "perfect" at being a predator?  Would it mean:

Fastest possible at chasing its prey? But it just needs to be faster than the prey, if it even bothers to chase its prey. Sea anemones are predators.
Most exactly adapted to hunting a specific prey? Are anteaters a near-perfect predator?
Deadliest possible poison? But many effective predators don't bother with poison.
Using the minimum possible energy to catch its prey? Are passive predators like pitcher plants nearly perfect?
Impossibly smarter than its prey? But it doesn't need to be smart. See again the pitcher plant.

Perhaps humans are the "perfect predators" because we've so dominated our prey that most of them live and die entirely at our whim, to the degree that many of us are barely even aware of them until their flesh is delivered to our dinner plate.
I hope I've made my point here, that the notion of a perfect predator doesn't really make sense biologically. Mostly, I think it's just a narrative idea of "thing that people would find really scary if it was hunting them."

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


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Why are people not given every possible vaccine?
Vaccines for some diseases, like cholera, are not given in Australia because of how rare they are. Nonetheless, I don't see the harm in giving a cholera vaccine to every child like we do got Hepatitis B. If there's no harm, why not just give children vaccination against every single disease we can? Just for safety's sake. What if a child happened to get cholera whilst playing in a bin and caused an outbreak?
Is the reason why this is not done just because of cost?

Vaccines cost money, and can have side effects.

Lots of in depth info here, starting from the third result down: https://www.google.com/search?q=pros+and+cons+of+vaccine+programs&oq=pros+and+cons+of+vaccine+programs&aqs=chrome..69i57j33i10i160.5147j1j4&sourceid=chrome&ie=UTF-8

Every public health decision is a cost-benefit decision involving at least two considerations:

Will the positive benefits of this intervention outweigh the potential harms?
Will the money spent on this intervention produce more benefit if spent on a different intervention?

Some vaccines, like the measles vaccine, are extremely safe and long-lasting, so it makes sense to give them universally. Others are less effective, less safe, or last for a shorter time, and so it just isn't worth it to give it to people who aren't likely to be exposed to the disease.
In the particular case of the cholera vaccine, it appears that it rapidly decreases in efficacy, even over the course of a single year. Mass inoculation of a population unlikely to encounter cholera before the vaccine becomes ineffective thus is not a particularly good use of resources.


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Are there any online resources for finding the signaling pathways that two proteins both belong to?
I am studying the proteins GSK3 and AMPK and I am trying to identify the signaling pathways that both of these proteins belong to. From reading journal papers I have found out that both of these proteins belong to the mTOR signaling pathway. I know on KEGG if you type the name of a gene involved in a signaling pathway (e.g. GSK3B) in the search bar on the page showing a signaling pathway (e.g. the mTOR pathway), you can find more information about that gene. However, I was wondering if there are any resources online where you can type the names of multiple genes and you can find out the signaling pathways that all of the genes are in?
Any insights are appreciated.

I would try "gsk3" AND "AMPK" at WikiPathways .
Here are some pathways where both GSK3 and AMPK are participants, such as:

And


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Why do water molecules diffuse along axons direction?
I am studying tractography technique which aims to reconstruct bundles of axons in brain by following the diffusion direction of water. It is very interesting because it is non-invasive. It exploits the difference between grey matter and white matter: in white matter (axons) we find an anisotropic environment since there is a preferential direction of diffusivity of water molecules that is along the axons direction, while in grey matter the environment is isotropic since molecules do not move with a preferential direction. The diffusion of molecules is generally given by a difference of concentration of molecules between two points but they should move even though this gradient is not present because of the temperature so because of the fact that they have a certain thermal energy. Therefore my question is: why do molecules move along the axons direction ? Is there a biological aspect that causes like a difference in concentration between the starting point and the ending point ? Maybe the answer is trivial but since I am not a biologist I do not know it :) and I am not able to find something on web . It seems that I find only explanations for diffusion of water molecules from outside the cell to inside... I would like to know the reason why they move in the same direction of the axon.

The movement is just the thermal energy motion you describe, not due to any concentration difference.
The anisotropy is due to the geometry. White matter tracts are effectively a dense bundle of thick, fatty hoses. Water can freely move in the tubes but cannot move as freely through the dense walls, so you see more movement along the axon length rather than perpendicular to them.
You can read more at https://en.wikipedia.org/wiki/Diffusion_MRI


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Do whales ever just hang out on the surface breathing?
You only ever hear of whales surfacing for a brief second to exhale/inhale before they dive back down. But do they ever just stay at surface level, laying there with their blow hole up in the air, continuously breathing for a while? One would think that might be a relaxing experience for them?

Whales often hang out on the surface for a while, for a number of reasons. Sometimes it is for curiosity, sometimes to socialize with other whales, and sometimes simply to rest.  The particular sort behavior that you are describing sounds like logging, where the whale basically rests, often for an extended period of time, with its back slightly out of the water, looking sort of like a floating log.

Cool, thanks alot!

From personal experience, I can attest to the fact that whales will hang out on the surface. Additionally, some species are more known among researchers/observers for this behavior. Kogia species (dwarf and pygmy sperm whales) are notorious for logging, for example. This study from Hawaii mentions that dwarf sperm whales spent a considerable amount of time in encounters either slow rolling at the surface or logging.


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Why do insect legs look so different from mammal legs?
Why do insects (and spiders and centipedes) have legs that are angled acutely upward then downward to meet the ground whereas mammals large and small all have straight legs that curve only slightly when walking or running? Why are they so different in morphology when they serve exactly the same function, i.e. load bearing and level attitude keeping of the central torso when in rest and motion? If the larger mammal's leg is evolved to favor large ground clearance for eyes to better spot threat/prey, then how come very small rodents also have straight legs when they should evolve to favor rapid gait because they are so small that they can not stand above grass or most obstacles in nature?

Evolution is based on chance.  AFAIK, the ancestors of arthropods and vertebrates diverged before legs really evolved.  From there, whatever bunch of random changes that improve fitness get adopted.  (And not all arthropod legs fit that insect architecture: for instance millipedes.)

You're up against the square/cube law. That is, body mass increases as the cube of size. That means that the larger an animal is, the stronger splayed-out insect-style legs would have to be, and the more muscle power is needed to support & move them.  For example, try doing a pushup with your arms extended out to the sides: it's a LOT harder than the normal arms underneath you one, isn't it?

Evolution includes chance, but it's not based on chance.

Plus one for point 2.


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Alkaline Phosphatase and Ligase Protocol for Cloning

In the image the circular molecule is a restricted vector and the linear red molecule is a DNA insert.
I found this protocol in my lessons notes, but I don't understand how it is possible that ligase catalyzes a reaction between 5'-OH and 5'-P. This reaction should form as product a 5'-5' bridge between the 2 nucleotides of the insert and the vector.
Usually Ligase repairs nicks between 5'-P and 3'-OH thus creating 5'-3' bonds between nucleotides that are normal in nucleic acids, so my question is how is it possible for the DNA to be functional even though it has a 5'-5' bond?

DNA ligase catalyzes the formation of a bond between 3’-OH and 5’-PO4 of its nucleic acid substrate. (See Lehnman, 1974) The ligation bond will be formed when the proper ends are close together, allowing the ligase to act. Lets redraw your diagram and add the 5’ and 3’ designations to it. I think this may help clear out some points.

Regarding the alkaline phosphatase treatment with ligation, I think Dale and Greenaway said it so much better than I can. Quoting (Dale and Greenaway, 1985):

[The strategy] is to treat the cleaved vector DNA with alkaline phosphatase that removes the 5’-phosphate group from the DNA. Since the presence of a terminal 5’-phosphate is necessary for the action of DNA ligase, a dephosphorylated DNA strand will not be able to participate in a ligation reaction. Since this will apply to both ends of the linearized vector, the ends cannot be joined together again, i e , parental vector regeneration is impossible. This results in a very low frequency of transformation by the vector (since linear DNA transforms very poorly). However, the vector 3’-hydroxyl ends are available for joining (by DNA ligase) to the 5’-phosphate termini of any DNA fragments to be cloned. This will result in a circular recombinant molecules with a single-stranded nick at each end of the vector portion. These molecules usually transform as efficiently as the fully ligated product, and the nicks are repaired in vivo after transformation. Thus the phosphatase treatment of the vector molecules increases the proportion of hybrid DNA molecules in the population of transformed cells, and also prevents the formation of oligomeric forms of the vector.

References
Dale, J.W. and Greenaway, P.J. (1985) “The use of alkaline phosphatase to prevent vector regeneration” Methods Mol. Biol. 2:231-236. Link to paper
Lehnman, I.R. (1974) “DNA Ligase: Structure, Mechanism, and Function” Science 186:790-797. Link to paper


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What is the difference between non-coding and intergenic regions?
The initial question was about understanding what is in the downstream of a gene in a eukaryotic organism. I understand that this region is located 3' of a gene, and therefore I would expect to find non-coding regions, but is there a difference between non-coding regions and an intergenic region?
A small background of what I am doing: I am studying the effect of retrotransposons in S. cerevisiae populations, and I already identified the potential impacts of these retrotransposons and these were the consequences:
Upstream gene variant   49
Downstream gene variant 42
Intergenic variant  4
Transcript ablation 3
Coding sequence variant 1
Feature elongation  1
3' UTR variant  1

So is it clever to say that downstream of a gene there are non-coding genes?

There may be non-coding regions (introns) within a single gene.

But up/downstream of a gene should not consider the introns as these are happening within the gene.

"Intergenic" is, well, an embarrassment, though it can be hard to avoid.  Intergenic means, literally, between genes.  Genes are, as you'd expect, genetically defined as regions of the chromosome with some genetic role.  Between genes, we have, well, junk, spam, without meaning or significance, since otherwise, it would be a gene.  In the 1990s everybody knew most of the genome was "junk DNA" and it was pretty straightforward.  And the central dogma was DNA makes mRNA makes protein and if there was no mRNA making protein, or even no long protein, then they assumed there was no gene.
Well, the problem with using these terms nowadays is, first, it is very hard to show any given piece of DNA never has a role.  After all, you can often remove a whole gene without visible effect on an organism, so how can some noncoding sequence 'between genes' be proved conclusively to be meaningless and of no relevance to either of its neighbors?  And second, DNA definitely does have a role even if all it does is produce non-coding RNA, or act as a regulatory sequence that does.  So for example, on OMIM you can look up many records for "intergenic", with results like H19, for which one term is "LONG INTERGENIC NONCODING RNA H19".  Note also H19 is listed as the HGNC approved gene symbol, so it is an intergenic gene.  Tricky, eh?  (I have great respect for OMIM - this isn't their fault)  Also, enhancers can be quite a long way from a gene, even past the end of another gene or affecting multiple genes, so even though a mutation in the enhancer might genetically act as an allele of a specific gene, it might be described in sequence terms as located in an intergenic region.
Bottom line: the intergenic regions you're reading about are going to be between things that are recognized as genes, and may or may not be known to have some effect on one or the other (or both...).  They won't contain CDS, which is always considered to be a gene, nor 5'UTR or 3'UTR because those are transcribed before or after a CDS.  Past that, how they are being distinguished from "upstream sequence" and "downstream sequence", that could be completely arbitrary.  They might have gone to WormBase and pulled out curated gene records, and added some number of base pairs before the start site as promoter - but I don't know that.  You'll just have to try to find the particular reference for whatever tool you are using.

An intergenic region is just one of many types of non-coding sequence.
Others include:

promoters
regulatory binding sites
terminators
introns
aptamers
ribosome entry sites

There's a lot of stuff that's part of genes besides the protein coding sequence.
A good way to get a picture of the sorts of things there are besides coding regions is to browse the Sequence Ontology.  If you browse to coding sequence and start browsing parent and cousin terms, you'll find a vast number including all of the things that I mentioned above, as well as intergenic region, with definitions associated with ear.

correct me if I'm wrong but poly-A sequences are not coded into the DNA, they are the result of RNA processing

You're right; the poly-A attachment site gets marked, but it's a junction and not a region; I've dropped it from the list.


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Does lack of adaptations for sperm competition necessarily shows the species are monogamous/serially monogamous/polygynous?
On the one hand adaptations for sperm competition, such as large testes, mate guarding, etc. are used to support that female in species are promiscuous.
On the other hand we know multiple eusocial species where most inidividuals don't reproduce letting their kin (e.g. the bee queen) reproduce. Which means that in some cases it is more beneficial to let your kin reproduce than to do it yourself.
For that matter, would not there be intermediate states, where multiple indivuduals reproduce, females are promiscuous, but since reproducing as much as possible yourself is not necessarily good, sperm competition adaptations would not get developed? Are there any candidates for such species?


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How do short polypeptide chains serve as identifiable antigens?
My understanding is that MHC class I and II bind to relatively short polypeptide chains (~ 20ish amino acids). I'm surprised that a non-self protein fragment that short would be distinctive enough to target for an immune response. Also, how does expressing one polypeptide chain help the immune system identify the source? Isn't it quite likely that the presented polypeptide is in the interior of a protein and would never actually be exposed to the environment until after it's been lysed? Or is it hydrophilic peptides that bind?


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Characteristics of 'true' tissue
Why are sponges not considered to have tissue level organization?
Quite a few places seem to say that sponges do not have 'true tissue' and only have specialized cells.

Unlike Protozoans, the Poriferans are multicellular. However, unlike higher metazoans, the cells that make up a sponge are not organized into tissues. Therefore, sponges lack true tissues and organs;

The Wikipedia page on sponges says -

Sponges are similar to other animals in that they are multicellular, heterotrophic, lack cell walls and produce sperm cells. Unlike other animals, they lack true tissues and organs.

I have not been able to find what defines true tissue, so I would like to understand what characteristics a group of cells must have for it to be considered proper tissue.

Can you please expand your question with at least one quote from a source that uses the term "true tissue", in order to help understand your question? When I google, the term I find is "organized tissue", which may be different than you are asking about.

@jakebeal I'm so sorry, I don't really know how you add a quote from a source. However, true tissue is what showed up on multiple pages when I googled 'Do sponges have tissues and organs?'

Is this the definition you mean https://glossary.lias.net/wiki/True_tissue ?

@ani You can edit your question and add text from one of the sources that you saw.  To indicate a quote, you can just use quotation marks or do a ">" for a blockquote.

@jakebeal thank you! I've edited the question, hope it is clearer now.


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Why can't plain water be used in dialysis? Why is buffer used?
I read that buffer is used in dialysis because usage of water could cause precipitation of proteins but I don't really understand why and how water can cause precipitation of proteins and buffer cannot.

I read that buffer is used in dialysis - where did you read this? The context of a direct quote would be helpful.

In my teacher's learning materials.


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How does pressure travel through the cochlea exactly?
I cannot find this answer anywhere.
What I do know is that the stapes pounds on the round window of the cochlea and this causes the fluid to move inside the cochlea itself, which has the three chambers (the scala vestibuli, the scala media, and the scala tympani), where the basilar membrane between the scala media and scala tympani is what fluctuates with pressure. This leads to the sound processing in the scala media and the organ of Corti due to the shearing motion of the hair cells against the tectorial membrane, and so on and so forth.
But I don't understand the pathway of the pressure. A lot of resources show the pressure wave moving front-to-back (towards the apex), making the basilar membrane move simultaneously. But at the same time, they also show that the full pathway through the cochlea goes front-to-back through the scala vestibuli, turns around at the apex, and then goes back-to-front through the scala tympani where the basilar membrane is located. So how can the basilar membrane be moving front-to-back when it's stretching along the latter half of this cochlear pathway, way over on the other side of the scala media?
Therefore I am unclear if (1), (2), or both of the following are true:
(1): Does the pressure somehow permeate through Reissner's membrane (between the scala vestibuli and scala media), move through the scala media (without disturbing any hairs in the organ of Corti), and then push on the basilar membrane from above, which would allow for this front-to-back wave motion?
(2): Does the pressure move the basilar membrane from below during its "return trip" going back-to-front through the scala tympani?

Short answer
The pressure wave through the scala vestibuli drives the basilar membrane response (BM). Your option (1) is correct, (2) is not. The pressure not really permeates or penetrates Reissner's membrane though; it is the pressure differential across the scala vestibuli and scala tympani that is the driving force for the BM movement.
Background
The most accepted way of viewing acoustic activation of the auditory system is the traveling wave theory (Fig. 1) as posed by the famous experiments of Georg von Békésy in the 1960's. These experiments showed, basically, that the basal part of the basilar membrane (BM) starts vibrating first (near the cochlear 'entrance' at the round window) and as the wave travels through the scala vestibuli, more apical parts get activated (Fig 2). This phenomenon explains the cochlear delay that's seen, i.e., that low frequencies tend to activate hair cells later than high-pitched sounds do (He and Ren 2013).
Reissner's membrane separates the scala vestibuli from the scala media. The traveling wave generates a pressure difference between the scala vestibuli and scala tympani. As you rightfully say, this pressure difference is established across Reissner's membrane and across the BM (Fig. 3). It is the movement of the BM that ultimately results in the sensation of sound (source: Ento Key). In fact, the movement of Reissner's membrane is comparable to that of the BM (Reichenbach et al., 2012). However, Reissner's membrane is not tuned and contains no neural elements involved in hearing. The stereocilia of the hair cells are embedded in the tectorial membrane. The shearing forces between the BM and tectorial membrane eventually result in mechanotransduction (Fig. 3). See Fig. 12.5 on this web page from Neuroscience online textbook for an informative video on the BM movement relative to the tectotial membrane.
The traveling wave is basically confined from base  to apex. Because of the tuning of the basilar membrane, high frequencies resonate the basal part (because the BM is stiff and narrow) and low frequencies the apical part (because the BM is wide and floppy). Each time a resonant frequency is met, the BM starts vibrating maximally and basically the frequency cannot go further and its energy is dissipated. Thus, along the way, sound traveling through the scala vestibuli  to the helicotrema (the boundary of the scala vestibulu and tympani) more and more energy is used up from the pressure wave. Thus, the basilar membrane is set in motion primarily by the pressure differences occurring in the scala vestibuli and by the time the traveling wave reaches the helicotrema no appreciable energy is left as all auditory frequencies have been filtered out. Remaining energy containing frequencies outside the audible range (roughly 20 - 20,000 Hz) continue to travel to the scala tympani (think of static pressure during a deep dive) and therefore the round window is necessary to act as a buffer (Robles & Rugggero, 2001).
However, there are other theories, notably one from Hermann von Helmholtz, a brilliant scientist of the 1800's that has revolutionized sensory sciences. It is called the 'sympathetic resonance' theory. I am not at all familiar with this theory, as it has been largely abandoned, at least as far as I know. The theory from Von Békésy assumes that the basilar membrane is a place-to-frequency converter that acts like a Fourier transformer, known as the place coding theory. Basically, the traveling wave dissects complex acoustic stimuli into different acoustic frequencies by menas of frequency tuning of the BM (Fig. 2). By contrast, Helmholtz assumed there are tiny tuned elements positioned in the cochlea that basically perform the Fourier transform (not shown here). If you wish to read more of the latter theory, I happily refer you to Bell, 2004).

Fig. 1. Traveling wave. source: NY University

Fig. 2. Basilar membrane movement. source: NY University

Fig. 3. cross section through cochlear duct. source: Psychology Wiki
References
- Bell, Plos Biology (2004); 2(10):e337
- He & Ren, Scientific Reports (2013); 3: 1874
- Purves et al. (eds), Neuroscience (2001) 2nd ed. Sunderland (MA): Sinauer Associates
- Reichenbach et al., Cell Rep (2012); 1(4): 374–84
- Robles & Rugggero, Phys Rev (2001); 81(3): 1306-43


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Do plant viruses attack animals? examples?
Do plant viruses attack animals, if yes please give an example of the virus.
I feel both plant and animal viruses are different, and they cannot attack each other hosts.

Plant viruses attacking animals or vice versa would mean that an animal serves as a biological vector to a plant or that a plant serves as a biological vector to an animal (depending on whose prospective you take by considering it as the host). This is highly unlikely

due to very different properties of the plant and the animal cells, while the virus has to be adapted to replicating in both
due to the nature of the interactions between the plants and the animals which are unfavorable to transmission between viral habitats (unlike, e.g., direct blood exchange between an animal and a stinging insect).

On the other hand, plants and insects routinely serve as mechanical vectors for transmitting viruses: an insect feeding on one plant may carry virus particles to another plant, and similarly a plant may mediate viral particles exchange between insects.
See Viral Ecology by Hurst et al.

WRT different properties, note that many (most/all?) animal viruses are even more specific.  They attack only one or a few cell types in the animal.

@jamesqf indeed, but they can attack different species - e.g., a human and a mosquito.

But are mosquito-borne viruses actively infecting the mosquito, or are they just carried by it, in the same way that airborne viruses are carried in droplets?  That is, mosquito sucks some blood from an infected person, virus floating around in that blood gets transmitted to the next person bitten.

@jamesqf It depends on the virus and the insect. In your scenario the insect is still a mechanical vector - it only carried the virus. However some viruses do take active use of the alternate hosts. Flaviviruses (Zika, Dengue, Yellow fever, West Nile) are an example. Not only they reproduce in a mosquitor, but they can even be passed vertically to their progeny. On the other hand, there is no horisontal tarnsmission between mosquitoes for physiological reasons (mosquitoes do not exchange body fluids). It is still specific in the sense that it infects a particular species of mosquito.

Interesting.  I learned something new :-)


text:
Understanding the use of English tenses in biological journal articles
My colleague and I (second language speakers) got in an argument in understanding the sentence:  " however, how this complexity and diversification have been achieved remains rather poorly understood.” in the context of the below Abstract’s report.
In short, the question is:
Does this sentence valid till the end of this report? i.e. the complexity problem continued and not solved in this study?
His understanding that this sentence stated in this report as a past context or past story, i.e. the abstract is telling us how our knowledge was? and this study solved and answered how this complexity happens and achieved.
Reference:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1852327/
I know these questions are mostly about understanding English rather than biology!
I appreciate your help.

I’m voting to have this question transferred to English Language and Usage under the tab "technical" if others regard it as off topic here.

I regard this is more of a question for SE English Language and Usage under the tag “technical”, and will vote to move it there. However, as the answer relates to reading papers in molecular biology, I provide an answer here.
Linguistic interpretation without context
The tense used in the phrase “X remains poorly understood”, taken in isolation, suggests that this is the situation now. Hence, it is the situation at the end of the study.
However…
Interpretation in context
This is the Introduction section of the paper. In the Introduction to papers reporting experimental biological research, it is usual (and helpful to the reader) to explain the background to the study and why it was undertaken. In this case to explain that the incomplete understanding of the subject justified further studies such as the one to be described.
This is made clear at the end  of the Introduction, where one often indicates in a sentence what the work to be described adds to knowledge: “Our results show that flagellum originated very early, before the diversification of contemporary bacterial phyla…”.
So the minimal implication is that as a result of the work described “X is now better understood”. And that is clearly the case here.
This is borne out by the final paragraph of the Results section in which the authors emphasize the contribution to knowledge that their work has made. You don’t get published in PNAS by saying that you have left the field still in the dark!
Why not use a different tense and say that you the problem has been solved?
An alternative would have been to write:
“Before this work was undertaken X was poorly understood”
The reason for not doing this could either be “scientific modesty” (also known as don’t antagonize the referees by appearing arrogant) or acknowledgement that, despite the significance of the work presented, there are still aspects of the problem that are not understood.

Your Answer is awesome! Thank you very much

@A.Qatar I am glad that you found it useful. The form on SE is to "accept" an answer if you think it correct and has answered your question. This informs others that the poster thinks the question has been dealt with (so they can prioritize other questions) and rewards the person who answers. However, I think it is best to wait several days before accepting an answer, especially if you cannot be certain it is correct. A better answer may appear, or others may criticize the answer that seems at first ok, either by comments or down votes. So take your time.


text:
Will Saliva make food go bad
My mom was telling me that if I put the unfinished bowl of milk and cereal back to the fridge, the saliva that has been stuck to the spoon gets passed to the milk. The saliva in milk will make milk go bad faster than if there were no saliva inside. Is that true? If so, how comes? It would be great if there are scientific evidences or references to back it up.
I have found a Quora post having some people saying that it will make the food go bad faster. I was not able to find any other references

It is the bacteria in the saliva , not the saliva itself.

What research have you done on your own to try to answer your question? Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way.


text:
Is viral single-stranded RNA in the absence of reverse transcriptase infectious?
In a medical microbiology textbook I'm reading (Murray et al, 1994), the authors state the following:

The retrovirus genome has a 5' cap and is polyadenylated at the 3' end. Although the genome resembles a messenger RNA (mRNA), it is not infectious because it does not encode for a polymerase that can directly generate more mRNA. The genome consists of at least three major genes that encode for the enzymatic and structural proteins of the virus: gag (group-specific antigen), pol (polymerase), and env (envelope). At the end of the genome are long terminal repeat (LTR) sequences

From this, I interpreted that because viral RNA doesn't encode an RNA polymerase, it is not itself infectious. However, if a cell were to be injected with retroviral single-stranded RNA alone, wouldn't this RNA be translated into proteins (including reverse transcriptase) as if it were normal mRNA into a protein? If this were correct, then the single-stranded RNA has all the information in itself to propagate the virus. Single-stranded RNA needs to be reverse-transcribed into the host's DNA before being transcribed into mRNA that can be translated.
Is there something different between viral RNA and the mRNA transcript that makes one translatable and the other not?
Source: Murray, Patrick R et al, Medical Microbiology (1994), Second Edition.
EDIT/UPDATE
I contacted the author of this chapter (Dr. Ken Rosenthal) and gained some more insight into how this hypothetical (injecting plain retroviral RNA into a cell) would play out. His answer is that yes producing new viruses possible but not probable. The reasoning for this is as follows:

The main reason that a new virus would likely not be created is that for the genome to make a new virus, reverse transcriptase is needed. Without reverse transcriptase, cDNA can't be made. Suppose that a ribosome was able to make reverse transcriptase with naked retroviral RNA and this newly made reverse transcriptase stayed near the ribosome. It would have difficulties making new cDNA from the original RNA template. One of those challenges is that cDNA synthesis needs a specific primer on reverse transcriptase.
The translated retroviral RNA would likely be degraded due to their finite lifespan in the cytoplasm.
There would need to be enough viral proteins translated to form a capsid. This would be unlikely considering the lifetime of the RNA in
Even if there were enough proteins in the cytoplasm, these proteins would then have to remove the RNA from the ribosome to encapsidate it. This is also unlikely.

Considering this, the microinjection of naked retroviral RNA would be an inefficient process to cause an infection.

@F16Falcon — Could you indicate what relevance the article you cite has to this question?

@F16Falcon — But retroviruses do not possess self-replicating RNA and depend on DNA for their replication. So as far as I can see the article — which is on "The RNA World" — however interesting, would seem irrelevant to the poster's concerns.

So now compare the author's response to my answer. Despite my current score of –1, I do believe I was right. Perhaps you might consider giving credit where it is due and accepting it.

Thanks. It’s the principle not the points (which I have little need of.)

Sure thing, though I disagree with you on one particular point (namely that I shouldn't focus on hypotheticals and "injecting" RNA). I find hypotheticals a useful way to find interesting questions. All the best David.

As far as I can understand, the poster is concerned about the statement:

Although the genome resembles a messenger RNA (mRNA), it is not infectious because it does not encode for a polymerase that can directly generate more mRNA.

I find this a somewhat unfortunate aside as the infectivity or not of viral RNA “injected into a cell” has no physiological relevance, and would advise the student to focus on the essential details of the actual viral life cycle rather than on this sort of thing.
However, the point it would seem that the poster and the other answer misses is that numbers count. A virus (or viral RNA) needs to generate enough progeny for infection to overwhelm antiviral defences. This entails there being sufficient mRNA generated from the genomic RNA (or DNA) for translation into protein.
In the case of ‘normal’ RNA viruses (i.e. non-retroviruses), this involves an RNA-dependent RNA polymerase, which has to be virally coded as the host cell does not have such an enzyme. Retroviruses, however, produce multiple mRNA molecules from an integrated DNA genome (integrated through the RNA-dependant DNA polymerase — reverse transcriptase) by using the cell’s DNA-dependant RNA polymerase, not from replicating the transcribed mRNA.
All viruses rely on host protein synthesizing systems to translate their mRNAs. But a single retroviral RNA that can act as both mRNA or (part of) the genome can only generate enough coat proteins etc. to encapsulate it (or enough reverse transcriptase to reverse copy it). A situation unlikely to cause retroviral RNA to be infectious in this hypothetical situation. I imagine it is this that the authors of the text have in mind.
The student of this subject would do well to distinguish the different transcriptional enzymes involved in viral replication and learn to refer to them by their full names.
Reference: Coffin et al. Retroviruses (1997), available on NCBI Bookshelf

RdRP is virally encoded, but is not necessarily carried in a virion. Thus, the replication of many positive-strand RNA viruses literally starts with translating their genome on a ribosome and thus generating RdRP. In other words, such an RNA introduced to a cell is literally infectious - which seems to be the premise of the question.

@Vadim — "many positive-strand viruses". But not retroviruses which do not encode an RNA-dependent RNA polymerase, which was the premise of the question.

In other words, what counts is not the numbers, but how virus replicates itself and what genes it carries. Note that RdRP is not a precondition here: if retroviral RNA encoded the reverse transcriptase, the integrase, and the other proteins necessary for initiating the retroviral replication cycle, it would be still infectious.

@Vadim — So you disagree with the authors of the text and regard retroviral RNA as infectious?

I disagree with your explanation of why it is non-infectious.

@Vadim — There may be other reasons, but the authors of the book that the poster is trying to understand say that it is because of lack of a replicase or replication, from which one draws the inescapable conclusion that they regard the generation of many copies of a viral RNA as important for infection. So they think numbers are important, and it needed someone to explain that to the poster and those other six people who share his confusion.

The lack of replication means no copies at all rather than few (vs. many) copies. In other words, it is qualitative rather than quantitative difference. In fact, in your earlier comments you acknowledge that much - it is the total absence of RdRP rather than its low efficiency. But the formulation in your answer is misleading.

In RNA viruses with a single-stranded genome, this RNA can be positive or negative sense. Positive sense RNA is directly translatable by a ribosome, while a negative strand RNA cannot be directly translated and therefore non-infectious. It either has to be converted to a positive strand RNA with the help of an RdRP (RNA-dependent RNA polymerase, carried in the virion) or reversely transcribed into a DNA which then serves as the template for generation of translatable mRNAs. In either case, this RNA is non-infectious in absence of the necessary proteins.
Note that positive strand RNA has to be propertly capped in order to be translatable. This is also not always the case - some viruses generate or steal the cap from the cellular mRNAs once uncoated in the cell.
Another aspect worth mentioning is that positive-sense retroviruses usually code for their genes in multiple reading frames and make heavy use of splicing to produce their proteins. Thus, directly translating their positive sense RNA is not sufficient for infection.
From Chapter 3 in Viral ecology:
For plus-strand RNA viruses except retroviruses, translation of the viral RNA
follows immediately after uncoating. The viral RNA extruded from the capsid is then
used by the host translation machinery for directing protein synthesis (Fig. 9).
For all other viruses, whether of DNA or RNA genome, the step immediately following
uncoating is either transcription of the genome yielding functional mRNAs or
reverse transcription of vRNA yielding proviral DNA (retroviruses).

References:

Viral Ecology
Principles of Virology


text:
Are the foramina of Magendie and Luschka genuine defects of the ependymal epithelium?
Question:
Are the foramen Magendie (or the median aperture) and the two foramina Luschka (or the lateral apertures) genuine defects of the ependymal epithelium? So the ventricular lumen truly communicates with the subarachnoid space? If so, how is the defect maintained? Also, what do the boundaries of the defects even look like?
Context:
The fact that there can be non-pathological defects in an epithelium is jarring for me, because I have always been taught that an epithelium consists of an uninterrupted layer of cells juxtaposed against each other, limited by a basement membrane on one side and encasing a lumen or facing the exterior on the other side.
So really there are no 'holes' in an epithelium, and even structures that might look like a hole, such as ducts for a gland, are in fact just invaginations of the epithelium.
I've been able to apply this concept to understanding other anatomical structures with no difficulty. If the foramina of the 4th ventricle are really epithelial 'holes' then this is a major anomaly. In fact, I cannot think of a single example other than this one in which a normally developed, intact epithelium (and a basement membrane) has a 'hole' in it.
Also if this is the case, how is the defect maintained? As far as I know, epithelia, when penetrated by trauma, promptly close the gap and re-epithelialize. I believe a persistent epithelial defect must have some kind of supporting mechanism that forces tolerance to such defects.
Lastly, I know almost nothing about cell polarity, but I've learned that that the surface of epithelial cells which faces the lumen is apically polarized, the surface facing neighbor cells is laterally, and the surface in contact with the basement membrane is basally polarized. Would cells at the boundary of the defects have their apical and basal surfaces directly in continuation with each other without an intervening lateral surface, having no neighbor cells to contact?
I've been searching the literature for quite a while, but nobody seems to be really bothered like me by the implications of holes being present in a normal epithelium. Perhaps I'm taking it too seriously and all that 'epithelia are uninterrupted layers of cells' talk is just a rule of thumb, a crude generalization meant to serve only pedagogical purposes. But these foramina of Magendie and Luschka are the only counterexamples to this maxim I could come up with so far. I believe that a rule this widely applicable must have some physiological basis, and therefore that deviations from it demand explanation.

I assume the opening would be contiguous with the arachnoid but I have failed to find any histological images or descriptions that demonstrate this.


text:
Exact average molecular weight of a dsDNA basepair
I am trying to calculate the exact weight of a given dsDNA.
On the Internet and the literature, different values for the av. molecular weight of one basepair are given :

660 g/mol (probably wrong),
other sources say 617.96 g/mol
Thermofisher gives 607.4 g/mol
(https://www.thermofisher.com/de/de/home/references/ambion-tech-support/rna-tools-and-calculators/dna-and-rna-molecular-weights-and-conversions.html)

I tried to calculate the average weight using following molecular weights:

molecule
.
weight

2'-Deoxyadenosin- 5'-monophosphate
dAMP
331,22 g/mol

2'-Deoxycytidin- 5'-monophosphate
dCMP
307,197 g/mol

2'-Deoxyguanosine 5'-monophosphate
dGMP
347.2212 g/mol

2'-Deoxythymidine-5'-monophosphate
dTMP
321.2005 g/mol

water
H2O
18,01528 g/mol

adding the matching nucleoside monophosphates together and subtracting one water for each peptide-bond condensation (one on the sense; one on the antisense side);
I get following formula for the average dsDNA basepair weight:
$$
avg.BP.weight = \frac {(dAMP+dTMP-\ce{2H2O})+(dGMP+dCMP-\ce{2H2O})}  {2}
$$
resulting in :
$$
\frac {(331,22+321.2005-36,03056)+(347.2212+307,197 -36,03056)}  {2} = 617.3892 \frac{g}{mol}
$$
which is very close but still 0.57081 short off the "best" literature value.
What am I missing?; Im trying to get this calculation as exact as possible.
Maybe i didn't consider some hydrogen or protons in bonds?
Thank you in advance!

The different protonations forms are considered in the averaged Mw.
Removing two H2O is the step that makes your average different than the traditional 650Da per base pair. But you must remember that the last base pair in the sequence will have it's OH group so you need to add 17.008 gr/mol * 2 = 34.016 gr/mol.
The effect of this changes with the length of your sequence, here is a graph showing it.

Blue line is your calculation and red line is the one from literature.
Literature one is achieved around 60bp (I calculated Mw(63bps) = 617.93) and yours at 10^6.6 (Mw(10^6.6) = 617.3892085)
Why you need this calculation to be so exact? Knowing the length of you sequence and region can help. Remember that some regions are richer in one type of nucleotides (CpG islands, hairpin coding sites)

Thank you for the precise answer and the great plot! I did this out of pure curiosity - I recognized that there where some inconsistencies (more generalizations) in the literature data so i tried to do my own calculations. I wrote a script to calculate the weight of an input sequence. My next goal would be to try to add the molecular weight of histones, linkerDNA , chaperones and the centromer, to calculate the total theoretical weight of the chromatin during metaphase. However i have now idea how to include variables like methylation. If you have further advice i would be truly thankful. :)

@user12256545 I try to be as doubtful as I can while modeling. If X happens in N stage how do I know it still happens in N+1 or K stage (everything in biology makes sense in retrospect but rarely in advance). Send me a message if you have code you'd like me to look at


text:
Most optically transparent muscle phantom?
I am trying to use Schlieren imaging techniques to visualize how a sound wave propagates through muscle tissue.
In the past, when needing to experiment with muscle we would use an agar based muscle phantom but they diffuse light. Might anyone have experience with making tissue phantoms that have similar clarity to something like PDMS for example?


text:
Numbering amino acid residues
While reading about primary structures of protein, I came across the following image.
What do the numberings $n-1, n, n+1$ in the below image refer to?
I thought about it : The amino acid residues are numbered from 1 to n starting from the N-terminus to the C-terminus .
But the image below shows only a part of the protein.. so why is the last residue numbered $n+1$ instead of $n$ also, why is this shown as termination?

I looked out few papers.. but they seem to be very technical and beyond the scope of my understanding.

Could you add the resource where you find the image?

@Hachiloni Actually, it is in the Grade 11 Biology Textbook (NCERT-India) (Old-edition) You can visit this link https://ncert.nic.in/ncerts/l/kebo109.pdf (Page-9)

This is a question of general scientific semantics. As you say, the image shows an internal region of a protein and is concerned with a tyrosine residue there. It is of no interest to know the absolute position of the tyrosine, but apparently necessary to refer to neighbouring residues. To do this one refers to the tyrosine residue as n so that one can refer to those on its N-terminal side by a minus designation with respect to it, and those on its C-terminal side by a plus designation. The termination (as you call it) is NOT shown. The C-terminus (noun) would end in COOH or COO–.

The image and the text accompanying it are rather confusing, especially to someone in high school biology. I think what it's trying to show is that amino acid (AA) residue numbering starts at the N-terminus (position #1) and continues to the C-terminus. If you are referring to a particular AA, you use its position - Tyr103, for example, and if you want to refer to a residue that's two positions toward the N-terminus, you would subtract 2. If you're going toward the C-terminus, you would add 2.

@David, Actually I interpreted 'n' as the last numbering and thus thought it as termination. It's clear now. Thanks Sir!

@MattDMO, Got it! Thank you Sir!

I don't understand why the question is downvoted! :(

This question is a bit hard to answer for me without more context.
However, it is clear that the n refers to the tyrosine which is highlighted in the figure as well (especially the interaction of its phenol). The other positions (n+1, n-1) are shown relative to the tyrosine.
I'm unsure about the role of tyrosine in the primary structure of proteins, but maybe this is more clearly explained where you found the figure. I'm also unsure if the glutamic acid is terminal.

Thanks! But even the textbook doesn't provide any explanation for this :( . One question, is it like we can show the positions of other residues w.r.t to a particular one? If that is so, this will suffice me.

Yes we can. The same is true for nucleotide sequences. (This is done in the fugure, too.)

Okay! Thanks for the input.

The textbook uses this as an example of the primary structure (amino acid sequence) of a peptide, but it doesn't say why.  The reason is that for many protein-protein interactions, the overall shape of the protein (secondary and tertiary structure) plays a very clear role ... but for post-translational modification of tyrosine, serine, and threonine residues, the sequence of amino acids immediately surrounding the amino acid to be modified has a particularly important role.  When tyrosine is to be modified, the relevant enzymes are tyrosine kinases, which attach phosphate at the -OH of tyrosine, and tyrosine phosphatases, which reverse this.
For consideration of the specificity of such enzymes it is quite common to align the substrate peptide sites with "n" or "0" being the position to be modified, and "n-1" or "-1" being the amino acid before it, and so on.  You can see an example for E. coli here .. not the most common place to look for this phenomenon, but interesting.  In humans there are 90-100 enzymes of each type, making these changes to any well-exposed part of a protein consistent with the specificity of that protein, with regulatory effects on the actions of many proteins that include causing them to interact with many other proteins, which contain SH2 domains, which also are targeted largely by the primary sequence around the tyrosine.  So these modifications are changing protein activity and associations in a complex network.  I think of it as a biochemical protein counterpart of the nervous system, due to the complexity of interactions that can be produced.  Note also that these phosphotyrosine sites are very easy to evolve by mutation of very few amino acids, allowing them to be introduced into new proteins to create new regulatory networks as needed, even in organisms with a long time between generations.  (They are an example of how "evolving evolvability" has been crucial to permit the evolution of large, complex, long-lived organisms)
For biologists, the most accessible piece of information is looking at the primary sequence surrounding each phosphorylation site, so this does make a relevant example of the concept ... but it would be too hard to explain it at that stage of instruction.

Thank you Sir! I get a fair (clear :P) idea of that now. +1 for your effort!


text:
What statistical test would you recommend to compare two animal behavior sampling methods?
I am doing a lab where I am comparing the scanning method and focal animal method. Each method will give me the following:

Scanning method: occurrence frequency for each behavior (%),
focal animal method:the occurrence frequencies (%), as well as the duration for each behavior.

I was thinking a chi-squared test or a t-test somehow but I'm not sure which to do or how to format them. Should I somehow compare the occurrence frequencies?
Not sure if this info is useful, but I normally use R for my statistical test but have never used my own data, only example data. I was going to record my data in excel and import it into R. Thank you in advance.

What do you want to compare between the methods? If you want to decide which is the correct method to measure, statistics isn't the answer. You need to consider the accuracy you obtain with each method, the objective, the data achieved, the resolution and your sample size. among other paremters

I agree with @Hachiloni that you seem to compare apples and oranges. The two methods provide you with different information, i.e., you measure different things. Perhaps, you could give more background about what you are doing, which could help to understand your problem better.

Also agree with Hachiloni. I think that we need more details about your experimental setup or study system. The question is not how to analyze the data but which addresses your study question. For example, I might ask why you don't take a video of the whole population and then do a focal analysis on each individual at every time point. Likely there is some technical difficulty with this, but it's really hard for us to tell!


text:
Why do we use mice in labs?
Why do we use mice in labs for experiments targeting humans ? Are they near humans biologically speaking ?

Interesting question in principle, but what research have you so far done to find an answer? It's a question that is addressed pretty much in every introductory textbook. In short, mice are often not good models for humans, that is indeed a big problem. But often it is not ethical or even possible to do experiments with humans (you're not allowed to insert things into peoples' brains, for example, or kill and dissect them), so animals are the only option. And animals can be bred to have specific characteristics.

Maybe start by skimming Wikipedia's page on Model Organisms, then edit your question with any specifics that remain unanswered?  Jamesqf covered a few pragmatic reasons, but there are a lot of other ones

Quite apart from ethical issues*, there's simple practicality.  Mice are about the smallest & fastest-reproducing mammal.  Mouse generation time is about 10 weeks, vs maybe 15 years for humans, and have average litter sizes of 6-8, vs a bit over one for humans.  Life span is correspondingly shorter, so experiments can be done over the entire life, or for multiple generations.  Mice occupy a lot less space, and are a lot cheaper to feed, which is a consideration when applying for research grants.
(And in the early days of research, one could just catch wild mice, instead of having to ship in some exotic species such as monkeys.)
*Which not everyone subscribes to. We do have ample historical evidence of humans used as lab animals.

you explain why this is a good model organism, but not why it is used in research targeting humans.

@Hachiloni: I DO explain that.  Because they're cheap, obviously :-)

algae are also cheap but you can study them to understand humans. Why mice are suitable for that?

@Hachiloni: Mice are mammals, algae are plants.  The biology is considerably different :-)  It's a matter of optimizing cost vs relevance of results.  You'll find that a lot of research IS done with plants, or with fruit flies, because they're even cheaper than mice, and the biology being studied is similar enough.  Likewise other research needs to be done with different, more expensive, animals such as primates, and sometimes (as with vaccines) human testing needs to be done.

Comparing mice and macaques (as human models and practicability for labs) would be interesting.


text:
How do we determine the common ancestor of a species?
I have seen a lot of articles about common ancestors. But I didn't find any perfect articles that said about the evidence of common ancestor.

https://www.khanacademy.org/science/high-school-biology/hs-evolution/hs-phylogeny/a/phylogenetic-trees

What do you define perfect? Are you speaking about making phylogenetic trees or about the theory of evolution in general? If about the later, it is a theory (so no definitive proof) but with a lot of supporting data and biological value. As far as I remember this site does not try to convince about that theory, there is enough material online

What is your actual question? If you have read up on the subject what specifically do you not understand?

The most definitive conclusions about the common ancestor are made by comparing genetic sequences of the organisms, for which well developed mathematical/computational methods exist, see, e.g., Inferring Phylogenies or An introduction to molecular evolution and phylogenetics.
For distant species the genomes are rarely directly comparable, so that some ambiguities can exist. Therefore the existing tree of life and species classification are based on comparison of the ribosomal RNA, which is believed to be rather conserved:
rRNA is one of only a few gene products present in all cells. For this reason,
genes that encode the rRNA (rDNA) are sequenced to identify an organism's
taxonomic group, calculate related groups, and estimate rates of species
divergence. As a result, many thousands of rRNA sequences are known and stored in
specialized databases such as RDP-II and SILVA.

Note that this still leaves out the viruses, which are acellular and therefore do not have theor own rRNA.

Thank you so much.


text:
How long does it take to reset sense of smell?
I have noticed that when I go on vacation for several days and then come back home, there is a distinctive, relatively mild paint smell in my apartment complex. However, under normal circumstances, this smell is virtually unnoticeable to me.
What are the primary factors that cause us to become used to certain smells? And, is there any way to estimate how long it takes to 'reset' the sense of smell, so that these smells which we have become used to will again be obvious?

the term you are looking for is Olfactory adaptation or Olfactory fatigue https://en.wikipedia.org/wiki/Olfactory_fatigue#:~:text=Olfactory%20fatigue%20is%20an%20example,'out%20of%20the%20ordinary'.


text:
Why aren't the twin organs like both the eyes, ears, hands and legs lying both sides of a human body identical?
Both the eyes are not identical in geometrical shape and size i.e. physical appearances of both the eyes of a person are different from each other. The same difference is observable in both the hands, ears.
I don't know which causes the difference in geometrical shape and size of the twin organs in the human body.
Any explanation will be greatly appreciated.

Does it help to think about it the other direction - why would they be the same?

Well, both the eyes belong to the same person and develop under apparently similar conditions but they are geometrically different. I really don't know where this geometrical difference in twin organs comes from.

"Similar", not identical.

Well, which conditions must be identical so as the twin organs become geometrically identical? Doesn't DNA or other biological change influence geometry of twin organs?

"which conditions must be identical" - All of them. Which is pretty much physically impossible. If DNA influences geometry, you'd expect less variance within an individual than between individuals. I'd be pretty confident that if you go looking for this, you'll find it for the cases you describe.

Maybe a nitpick, but the paired limbs/organs generally aren't identical, they're mirror images.  Which might have some influence on development: perhaps the most obvious is human handedness, with the preferred hand being used more.

The topic you're looking into is fluctuating asymmetry, a broad field of study.  Among the free reviews this one is a bit old but well on topic.  The general idea is that there is "developmental noise", which is opposed by mechanisms for developmental stability.  The review covers a variety of conclusions people try to read in to these studies, often about the stresses on the organism or the mechanisms by which development is "canalized" to reach a specific goal.
The nature of the noise is usually presumed rather than proven, since many different factors are presumably adding up to make small differences.  We may assume (though I'm not always sure it is true) that mRNA, protein, and signalling molecules diffuse to reach their targets, which is to say they are subject to Brownian motion with random variations in timing.  The need for multiple factors to get together for a complex process like transcription or translation means that the number of copies of a protein produced under a given circumstance will vary.  An example of this in hypertrophic cardiomyopathy has been proposed to contribute to disease progression, due to random bursts of transcription in individual heart cells affected by the disease.

Body development is a complex process in which the interaction of a huge amount of molecules and the environment give rise to the final product.
In such a complex system is not surprising that some chaotic dynamics exists, and if so, small perturbations during the process give rise to not so small difference in the final product.
What is surprising is that, even with such a big complexity, the final product (like the two eyes) is a stable state.
So I think the main question is not what make them different, but how the development process achieves to generate symmetry.

The other answers talked about how asymmetry happens. Here I say my idea on why asymmetry could be beneficial. Focusing on left and right brain lobes, you see that the difference between these lobes give new functionalities to brain and these new abilities could be beneficial during evolution of the taxa. I think asymmetry which looks like stochastic, maybe in thousands and millions of years, little by little (and some times suddenly) make new (useful and harmful) inheritable functions.


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How do rats open a walnut?
What techniques do rats use to open a walnut? What are the traces they leave in nature?
I have a book on traces that wild animals leave in nature, but it only explains squirrels (splitting the walnut in two halves, using their teeth as a lever) and mice (gnawing a hole into the hull of the nut). I am interested in the two common European species of rats, brown rat (Rattus norvegicus) and black rats (Rattus rattus).

In this article targeted at pet owners, it is implied that rats open nuts by gnawing on them (similar to mice, I presume). There don't seem to be scientific studies on the mechanics of how rats open walnuts. However this interesting study did find that consumption of walnuts improves brain function in aged rats, which is fascinating.
Based on this, I would expect the traces left behind in nature to be similar to those of mice, although the gnawed hole would potentially be larger given the relative difference in tooth size between the two groups.


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Do airsacs contract and expand when birds breathe?
Something I was wondering. When birds breathe, do their airsacs contract and expand like the lungs do?
Also, if they do, do they contract and expand as much as the lungs do?
Thanks so much!

This borders on a homework question, have you tried googling avian respiration. http://people.eku.edu/ritchisong/birdrespiration.html

@John Yes. I watched several videos on the subject and read several pages. One mentioned the lungs contracting and expanding slightly, but none said anything about the air sacs.

They move air in and out of their lungs and air sacs by means of special muscles that move the ribs and sternum downward and forward, expanding the body cavity and causing inspiration, and then up and backward, contracting the body cavity and causing expiration.

Thanks Jitendra Singh! I would've upvoted your answer, but I can't right now.

@ArchduchessFerdinand I guess below the upvote button you would have the tick button. If you like my answer then click on that button and wait till it becomes green. Actually, this would mean you have accepted my answer. If you havve any problem you can write in comment

I was told I'm meant to wait two days before accepting an answer, sorry.


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What type of epithelium are the pancreatic Islets of Langerhans?
The human pancreas contains exocrine acinus cells (simple cuboidal epithelium) and Islets of Langerhans. Despite looking online I cannot identify what type of epithelium the Islets of Langerhans conform to (e.g., cuboidal, columnar, squamous). I'm confident it is not squamous due to the shape of the cells, but the distinction between cuboidal and columnar seems equivocal here.

I think the image you've attached lacks clarity. If you see the image below, you could say that the epithelium is cuboidal with central rounded nucleus.

Unlike the oval nuclei of columnar epithelium, rounded nucleus suggests that they are cuboidal in shape.
The image is from https://webpath.med.utah.edu/HISTHTML/NORMAL/NORM010.html

Welcome. Can you add sources to your claim and mention where the image was extracted from?

It is a fact that cellular morphology as well as the shape of nucleus will be taken into account when describing a cell as columnar or cuboidal. Due to the lack of clarity in the OPs image, I am showing this image as it is clearer to understand.


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Difference between a phototroph and a photosynthetic organism?
A quick search on google about the topic and the page on wikipedia did not help understanding the difference between these two related terms.

Practically, 99% of the time there is no difference when using one term or another.
More strictly:
A phototroph ("a thing nourished by light") is according to your wiki page:

It is a common misconception that phototrophs are obligatorily photosynthetic. Many, but not all, phototrophs often photosynthesize: they anabolically convert carbon dioxide into organic material to be utilized structurally, functionally, or as a source for later catabolic processes (e.g. in the form of starches, sugars and fats). All phototrophs either use electron transport chains or direct proton pumping to establish an electrochemical gradient which is utilized by ATP synthase, to provide the molecular energy currency for the cell. Phototrophs can be either autotrophs or heterotrophs.

and

If their electron and hydrogen donors are inorganic compounds (e.g. $Na_2H_2SO_4$, as in some purple sulfur bacteria, or $H_2S$, as in some green sulfur bacteria) they can be also called lithotrophs, and so, some photoautotrophs are also called photolithoautotrophs.

So the difference resides in that some phototrophs do not carry out photosynthesis, which is a specific set of metabolic functions (those that do $CO_2$ --> organic compounds). An organism that carries out photosynthesis is then a photosynthetic organism.
In other words, photosynthetic organisms are a subset of phototrophs.


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VDJ sequencing in mice, DNA or RNA?
I am wondering if anyone who is well versed with VDJ sequencing for TCR repertoire analysis (specifically CDR3) would know if DNA or RNA is a better starting material? We are looking at the effects of radiation therapy on immune system of mice. Thanks

DNA is typically easier to work with. Just make sure the cells you're working with have actually matured enough and undergone VDJ recombination.

I agree with @MattDMo Colleagues next door have done this with single sorted cells which where sequenced afterwards.

@MattDMo @Chris♦ how do you suggest one makes sure T cells have matured and undergone VDJ recombination?? I have looked at literature and seen one study that looked at clonal expansion 22 days after radiation exposure but they did not say why. Also, I have read that RNA is better to use than DNA since DNA won’t give you the antigen specificity you can see with mRNA expression. I have also seen that DNA can only show you the possible combinations of VDJ you could get as mRNA shows you the ones you did get, in real time.

I suggest you spend some time looking at the details of somatic recombination. Early during maturation, the V, (D,) J, and C protogenes recombine in the DNA to form the first version of the recombined TCR $\alpha/\gamma$ and $\beta/\delta$ chains (different protogenes combine in different ways in the different chains). These recombined sequences are then transcribed as mRNA - to my knowledge the protogenes are never transcribed. So, mRNA sequences should match DNA sequences.

The reason I gave my caveat is because if you just take a whole thymus and do single-cell sequencing, you'll also get immature T cells that haven't undergone recombination. Instead, I would use either blood-derived cells, or sort thymocytes using a marker that is expressed after recombination. I would choose blood, because some of the recombined thymocytes will die during further maturation, and probably shouldn't be included in your measurements of TCR diversity.


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What would be a single elegant-sounding word denoting controlled increase or decrease?
I am a biologist and frequently encounter the words 'upregulated' and 'downregulated' in the literature. Appropriately, these words are flagged by my browser spell-checker; they don't seem to be very widely recognized outside of the biology community, and I find them quite ugly.
I would appreciate any and all suggestions for (ideally) single words or concise phrases that convey the same meaning: increased or decreased in a controlled or causative manner by the action of some external factor.
A general use case: "In experiment A, we determined that gene B was upregulated upon exposure to toxin C, while genes D, E, and F were downregulated."
Of course I could say that 'expression of gene B was increased by/in response to...' but 'B was upregulated' is so much shorter. Surely, though, there must be some way to convey this concisely without using such an annoying construction as 'upregulated'.

Biologists  probably made up “up/downregulated” just because they could find no better fitting term.

Augmented and diminished?

Scientists and engineers often look for "elegant" solutions. More often than not they are forced to agree with Kepler's  in vino veritas remarks on his own theories...

I really think this is not a biological question but a matter of style, and style is subject to personal opinion. I have published dozens of papers, but so have other people, and whereas I believe in calling a spade a spade, others prefer to describe it as a manual excavation solution. And the context is relevant: in a results section I would say precisely what was observed — no upstairs downstairs — whereas in an introduction or discussion I would be more inclined to use broader terms. But I would use as many words as necessary (I hate one-word requests on ELU) and technical terms if need be.

There's a reason why you encounter these words so frequently - they are widely understood, concise descriptions that almost any biologist will understand immediately. Almost any other terms you use in their place will only serve to obfuscate the actual biological phenomenon you're talking about.
That said, I've seen the words overexpressed and underexpressed to describe genes that are upregulated or downregulated, but they're not any less cumbersome words, nor are they used any more frequently outside the domain of biology. There are also may be some connotations about the cause of the effect, so there may be subtle differences between upregulation and overexpression depending on who you ask. I don't think there's any better terms than upregulation and downregulation for describing an effect of increased/decreased gene expression.


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When does one decide to refer to a virus as a new variant?
I've read that SARS-Cov-2 has several variants, e.g.:

Can the U.S. keep Covid variants in check? Here's what it takes.
Novavax’s Vaccine Works Well — Except on Variant First Found in South Africa

When does one decide to refer to a virus as a new variant?

My research:

I looked at https://biology.stackexchange.com/questions/tagged/variant?tab=Votes
The question What determines when a virus becomes a “new strain”? addresses strain. Is strain the same as variant?

For those looking at the SARS-CoV-2 phylogenetic tree it is mainly about how lineages (becomes a clade once large enough) grow, propagate from locations and locations and split in sublineages. Sometimes one lineage deserves attention not only because of its growth but also because of its mutations, this was the case for the summer variants bearing spike and RBD mutations. 501Y.v1 & 501Y.v2 emerged in this context bearing most of the interesting features spotted in the summer variants: many spike mutations and deletions, long branch/accelerated evolution, exponential growth.

We use them as synonyms. However, variant is, in my view, more colloquial than scientific. Strains are in the literature often defined by their distinct genome compared to other strains of the same species (might be one base-pair substitution or more). In microbiology, including viruses, we often think of a strain as the proliferation of a single distinct DNA/RNA molecule.
https://www.sciencelearn.org.nz/resources/184-virus-strains


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In our 23 chromosome pairs, do the 2 members of the pair have distinct or virtually identical sequences?
I understand that we have 46 DNA molecules in the nucleus of our cells, arranged in 23 pairs: 22 autosomal and 1 sex chromosome pairs.
I have read in different sources that the pairs contain nearly identical members, excluding any mutations. I have also read that the pairs contain 1 member we inherited from our mothers and 1 we inherited from our fathers, which are different due to inheritance.
This seems contradictory, given that genealogical companies match up on the differences on these chromosomes.
My understanding was that meiosis creates sperm and egg cells that each carry 23 chromosomes - they are haploids. During the first steps of meiosis that creates the reproductive cells we have a combining of the parent's chromosome pair from their parents to create 4 daughter cells, each independently viable, where the recombination of the chromosome pair has occurred at somewhat predictable spots (for you perhaps :-) ) and that these spots can be related to genes. It is this step that give us our genetic variation between siblings for example. A new person's DNA is partially formed from any one of these highly varied daughter cell possibilities.
Fertilization combines the reproductive cells to produce the 46 chromosome zygote with is again diploid.
I think this understanding supports the second interpretation that our chromosome pairs are not 2 nearly identical DNA molecules but are distinct.
Have I got this right? Is there a missing process or a misunderstanding in my interpretation?

I think there is a bit of confusion about what is meant by identical/distinct.  Two genes could appear identical, or nearly so, yet have different functions, say by just swapping a couple of nucleotides.

I am referring to the sequencing of SNPs, not to the function or expression of those sequences. Do both chromosomes in a chromosome pair have nearly identical sequences of ACTG excluding differences due to sequencing techniques and/or trivial transpositions of the sequence number up or down.

Could you elaborate on why you think the two sentences are contradictory? Nearly identical does not mean completly identical. SNPs are real single letter diferences between individual chromosomes - and not just differences due to sequencing technique. Genes are just small functional sections of the long chromosome sequence. What has been explained to you about sequences of genes does directly apply to sequence of chromosomes. The diferences are small and yet very important.

@BagiM One source stated that the two chromosomes in a pair will be identical except for the possibility of a very small number of snp differences could be due to mutation only. I believe this to be contradictory to the statement that within a pair one chromosome comes from the maternal source and one from the paternal source as there is no reason to think the donors would contribute identical dna.  I suppose what I am trying to ascertain is if there is a process somewhere in the fertilization steps where the donor chromosomes recombine, e.g. mix, before they form the new individual's dna.

Homologous chromosomes (those that are paired up), excluding the sex pair are almost identical in size, shape and genes (members as you called them) present in them.
Genes determine traits and each homologous chromosome controls the same traits. The level of identity of a gene inside a population varies between genes. There are very conserved ones that do not change even between humans and yeast and others that vary alot event inside a species. This changes can be small in sequence length, a simple base (letter) swap or one deletion, and have a huge effect on the traits. This is how chimps and humans are very different but share 98.6% of their genome and humans are very similar and share 99.9% of their genome.
In summary, on the bigger scale homologous chromosomes are very similar (size, shape, traits inside), on the smaller scale homologous chromosomes have small changes that affect greatly.
EDIT: elaborating on when recombination occurs.
The zygote do not recombine the chromosomes it gets from it's parents. Each parent chromosomes recombine in the first step of meiosis. We do not expect them to be identifcal on the gene level (or the SNPs level). Each chromosome represent each paren't genetic material.
Lets look at parents A chromosomes
parent a Paternal: a-b-c-d-e                       parent b Paternal: a-B-c-D-e
parent a Maternal: a-B-C-D-e                   parent b Maternal: a-b-C-D-e
possible recombination  (a)                       possible recombination (b)
(a-I) a-B-C-d-e                                         (b-I) a-B-C-D-e
(a-II) a-b-c-D-e                                         (b-II) a-b-c-D-e
Now the child can be any of the 4 possible combinations (and obviously all other not shown). Let's say (a-I) and (b-II). This chromosomes do not recombine until they get to the meiosis stage.

I am asking about an individual, not a population. I do not use members to refer to genes, I use members to refer to the individual chromosomes within a pair. I am also not asking about the impact of a mutation of a gene's base pairs.

@Stephen  Is your question "In each pair of chromosomes, are the parental and maternal chromosomes nearly identical or very distinct?". If you want an answer about an individual we need background about him, otherwise he is merely a random sample from population with every possible pairs of parents. I think my answer shows that chromosomes are almost identical on the macro scale and slightly distinct (but not much) on the micro scale. If you elaborate more I could expand my answer

I think that if you need to know specifics about an individual to answer this question then the question is not clear as I am asking about the typical results of the general reproductive cycle.

This is an attempt to understand at very high level what the strands of DNA in each chromosome of a pair are expected to be. To reword it, looking at the sequences of SNPs of an individual's DNA do we expect the sequences of the 2 chromosomes of a pair to be (nearly) identical, e.g. because the maternal and paternal donor DNA was combined and then duplicated, or do they remain distinctly identifiable as maternal and paternal complete, undivided chromosomes?

I think you may have been trying to answer "in a chromosome pair is the location and function of genes identical on each of the 2 chromosomes", which I understand to be "yes".

@Stephen I expanded my answer, maybe know it is clearer

Between what you have added, and what was posted by swbarnes2 in their answer, I believe I now understand my confusion. The overall number of differences between the two donors of chromosomes will be small compared to the overall size of the chromosome. Enough to be distinguishable for genealogical purposes, and to affect the expression of particular traits, but ultimately small in number, thus the "nearly identical" comment is in fact correct and not in contradiction with the other interpretation. Thank you for your effort in making this clearer.

I have read in different sources that the pairs contain nearly
identical members, excluding any mutations

"Nearly" is doing a lot of work there.
You have a copy of Chr 1 from your father and a copy from your mother.  Your copies might have mutations as compared to your parents that happened either in you as you were developing, or in the gametes as compared to the stem cells they originated from, but most of the differences between your maternal copy and your parental copy were caused by long ago mutations that have been in your parents' families for generations, (we'd be more likely to call those polymorphisms, rather than mutations) not mutations that just happened.
Even with those differences, your two copies of Chr 1 are at least 99% identical.

I think now that you've hit on what I needed to understand. Although there likely are differences caused by who we inherited the chromosome from, which are useful to understand from a genealogical point of view, these sequence differences are derived from, to use your number, about 1% of the matches, thus, "nearly" could be considered accurate, "from a certain point of view".

Two major resources of genetic variation between siblings:
1- Random segregation of chromosomes during meiosis I. consider only mother: the mother has 46 chromosomes, 23 from grandmother and 23 from grandfather. during meiosis anaphase I, pairs of similar (homologous) chromosomes are segregated randomly. finally you have  egg cells with 23 chromosomes, some from grandfather and some from grandmother. this can make 2^23 (8 millions) different combination of chromosomes for egg, and 2^23 for sperm and 2^46 (7000 billions) different combinations totally.
2- Recombination of homologous chromosomes during meiosis I. which is exchange of chromosome pieces during meiosis I metaphase, and I see you know enough about it.
Also, there are other resources of variation which are out of the level of this question.

Hello and thanks for answering. I do understand the points you've made in point 1. I am curious about the other sources of variation if you care to leave a reference. I think my confusion arises in the fertilization step - whether or not the donor chromosomes "pair up" but remain intact as one source indicated, or if the donor chromosomes undergo random segregation and combination akin to point 1, and then replicate before forming the chromosome pair of the new individual. My original understanding had been the former.


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Does probiotics bacteria from yogurt live in the mouth too? Does it populate the mouth/throat or just the gut?
Yes I was basically just wondered this as I've taken probiotics in a pill form but those only go to the gut. I guessed the mouth needs probiotics too and I wondered if yogurt can accomplish that.
I also found conflicting stuff on the internet: some say enzymes in the mouth kill the bacteria in yogurt, others say yogurt helps bad breath for example which means it does have beneficial bacteria that live there in the mouth probably.

of course they do... the question is for how long.
Probiotics will tend only to affect the microbiome in the digestive tract for a while.  For yogurt supplemented with probiotics subjects microbiomes drifted back within 48 hours.  Depending on your diet the individuals can hang out for a while or persist.  Children, who tend to drink more dairy have a more persistent Lactobacillus signature.


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Can a person survive without platlets in the bloodstream?
Can a person survive without platlets or thrombocytes in the bloodstream, if I guarentee that the person is isolated and won't injure?
Any help will be appreciated. Thank you!

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

No. Platelets not only function to prevent overflow of blood from the body by making clots. A considerable increase or decrease in the platelets in the blood can cause thrombocytopenia. Thrombocytopenia is a disease with nose bleeding, red spots on skin, vomits of blood, pink-coloured urine and headaches as common symptoms. Also, even if an isolated environment is provided you cannot prevent slight injuries like acidity and dust particles in the air.


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Trying to identify a beetle seen in Ontario, Canada...and its babies, or parasites?
I'm trying to identify a beetle I took video of in July (around 2010) in the Muskoka region of Ontario, Canada. Attached below is a still frame.
I've done some googling and was thinking this was a Milkweed Leaf Beetle because of the orange and black stripes. This beetle however has an interestingly marked green head, and Milkweed Leaf Beetles appear to only have a black head.
I'm especially curious to know if the smaller insects on this beetles back are its young, or some type of parasite.

I've just posted the original video to youtube. It's right here: Beetle Video....and a GIF below

Nice photo - could you give a bit more detail on where/when you found it? Thanks.

Thank-you. This is from about 10 years ago - and was shot sometime in July in the Muskoka region of Ontario, Canada.

In the future, please [edit] your original post. Comments are ephemeral and often overlooked, so they should not be used to convey information important to answering the question. Thanks!

@OrbitRob can I convince you to save a bi of your video as a gif and upload that directly to your post here? www.ezgif.com makes this process very easy. (you can upload your video, crop the length, and optimize to make the gif <2mb so SE lets you add it. Hope you consider it. thanks!

@theforestecologist - haven't logged in for awhile! I added a GIF like you suggested. Happy Holidays! :0)

Thanks to pascal's answer, I looked at the genus Nicrophorus and agree that this is some member of that genus. (The spelling Necrophorus has been used in the past but is now deprecated.)  The 60+ members of this genus are commonly known as burying beetles or sexton beetles from their behavior of burying dead small animals to serve as nourishment for their offspring.
However, instead of N. vespillo, I think the species might be N. tomentosus:
(Photo: Judy Gallagher via Wikimedia Commons)
The most distinguishing feature seems to be the green or gold hairs on the thorax as seen clearly in the large version of OP's photo. These hairs or setae Wikpedia mentions as separating N. tomentosus from other members of the genus.  A common name for the species is "gold-necked carrion beetle". Two other photos of this species are here and here.

Great picture. I like how the mites have placed themselves 'in colour-co-ordinated formation" on the beetle's back! Thanks for your help and FYI i've just added a link to the original video below the main photo in my question. Rob.

I compared what I could see in the OP photo with the identification key given in The Insects and Arachnids of Canada Part 13 (online here), and can confirm this specimen as Nicrophorus tomentosus.

I think I agree with mgkrebbs that this is N. tomentosus but the members of this genus are all very similar to one another. The part of your question that inquires about the "smaller insects on this beetles back" is of interest. They are not insects, they are mites.
The behavior of these mites is called "phoresis" and there is a good illustrated article here about it. The mites are simply using the beetle for transportation to food. The beetle is better than the mites at finding dead animals and is able to fly. This species of mite has evolved the lifestyle of a "hitchhiker" on the beetle. They have therefore become dependent on the beetle, but they are not a parasite, because the beetle is not harmed. In fact, there may be some benefit to the beetle, which would make this a mutualistic relationship.

Great info. Much appreciated! ...and FYI i've just added a link to the original video (it shows the mites moving around) below the main photo in my original question. Rob.

First clue that the mites are not the beetle's young are they've got 8 legs to the beetle's 6.

re: "there may be some benefit", from the linked article: "[the mites] feed on fly larvae and nematodes, which are competitors of the beetle"

This is a beetle of the species Necrophorus vespillo (or a relative), very common beetles. It is parasitized by some mites. A similar picture as yours can be found on this page. I like it very much! We can see on the external page, that those little creatures are mites.

(Picture from wikimedia commons)

Thanks for your help Pascal and FYI i've just added a link to the original video below the main photo in my original question. Rob.