text:
Infectious deadly disease among free animals?
Sorry for the presumably naive question, I'm not a biologist and searched for that but didn't find a clear answer to this question.
What I would like to know if deadly infectious diseases are common also among free animals (I mean living free in nature, not in captivity)? Therefore I'm NOT referring to the transmission from animals to humans like covid, bird or swine flu, rather infections that have caused several deaths among animals living in a natural environment without affecting humans? Is that something quite normal in the animal kingdom too? Presumably also before the appearance of humans? Or does it not happen? Or is it rare but exists? Eventually a link to some article or paper on this would be welcome.

Just as a brief response, yes, it happens all the time. There are endemic infectious diseases in wild populations all over the planet. We are definitely not unique in that. Here is an interesting BBC story about some of them from several years ago.

As far as scholarly articles go, here is a collection of them from Acta Veterinaria Scandinavica on BioMedCentral.


text:
Long-term efficacy and absence of side effects of anti-covid vaccines
The question is about the methodology/biostatistics of clinical trials (I state this beforehand to avoid accusations of being an anti-vaxxer).
As multiple anti-COVID vaccines are offered on the market, the question naturally arises about their long-term efficacy and possible side effects. As SARS-CoV-2 virus has been known for a bit more than a year, neither of these could be tested directly, so one probably has to rely on indirect knowledge due to the experience in developing other vaccines. Given that multiple vaccines have been approved for a wide use, there should exist well-established procedures to assure their efficacy and safety.
The question is: how does one prove the long-term efficacy and absence of side effects during a short period of time (short in comparison to the expected duration of immunity and absence of side effects).
Update
As @MattDMo have correctly pointed in their answer, the absence of long-term effects is established in the last phase of the clinical trials, while observing cohorts of vaccinated individuals during a long period of time. @MaximilianPress, in their comment, has also correctly brought up the fact that this is done within the framework of survival analysis. In particular, this means that it is sufficient to follow the vaccinated cohort during several years to evaluate the side effects that occur during their lifetime, as the survival analysis keeps track of the sensored data.
Here we are dealing with a situation where such a study could not be done - the best we can guarantee is the absence of the side effects in the next few months. We thus need to rely on a different method, which would account for the similarity between the established and the new vaccines.
I am less concerned about the vaccine efficacy, since the inefficacy of vaccines is usually against different strains of virus, as is in the case of influenza and Dengue.
Update 2
The accepted answer points out two important things:

The long-term side effects of a vaccine/medication can be truly understood only in the Phase IV of the clinical trials, i.e., after the vaccine is in widespread use.
The threshold for approving this specific vaccine is lower due to the emergency of the current health crisis.

This however still leaves open the question of the safeguards undertaken in the Phase III of the clinical trials, before the vaccine approval. I.e., the question is about ranking the candidate vaccines against the above-mentioned threshold.
Remarks:

I understand why this question irritates, but I believe that it is not the asking, but rather refusing to seek the answer that plays in the hands of anti-vaxxers.
I did follow the suggestions in the comments to pose this question in the medical and the statistics communities, but it seems to get there even less traction.

Update 3
Recent suspensions of Astrazeneca vaccine in 9 European countries demonstrate the importance of this issue.
Update 4 Pfizer vaccine has been fully approved - that is from now on it is considered a fully tested vaccine (till now it had been used under the emergency authorization).

What is your question?

I’m voting to close this question because this is a statement of opinion, not a question.

@David The question is: how does one prove the long-term efficacy and absence of side effects in such a short time.

@Vadim: One doesn't.  It is simply a question of whether the small risk of such long-term effects is less than the immediate risk of serious illness or death from the virus.

@jamesqf to make such a statement one has to estimate and compare the risks

Your question is then one of medical policy and public health, not a specific question of biology and is therefore off-topic here. It may be on topic on SE Medical Sciences, but you would be better to read one of the many detailed accounts available via reputable news sources.

Everyone, lets please be civil to one another.

I’m voting to close this question because it's probably more appropriate to SE Medical Sciences or a statistical forum. I believe that it is a question of how to handle censored data, but I'm not an expert in those spaces: https://en.wikipedia.org/wiki/Censoring_(statistics)

@MaximilianPress one cannot speak of "censored data" here, since there's no data to speak of. The risk-assesment methods are probably indirect, based on comparison with the existing vaccines, modelung, etc. But I am engaging in a guesswork here - which is why I am looking for an educated answer.

If what you want to ask is whether vaccines have long-term effects, then that is definitely a question for SE Medical Sciences. I guess that you can try to interpolate COVID vaccines somehow into the space of other vaccines, though it is starting to flirt with anti-vaxxers a little bit. It's basically asking "what is the long-term effect of an arbitrary strong immunologic challenge", except imputing that to an emergent property of vaccination. Maybe such emergent properties exist, but the place to get answers on that is from practicing vaccinologists.

@MaximilianPress as I explained in the update to my question, long-term effect of vaccines is my secondary concern. I think that knowledge is the best response to anti-vaxxers, although my mentioning of them has probably given a wrong direction to the whole discussion.

What do you mean with "This however still leaves open the question of the safeguards undertaken in the Phase III of the clinical trials"? General safety is tested in Phase 1, overall safety is also a part of Phase 3, here all observations are collected. So far, no serious side effects have been found. For long-term, Phase 4 studies are up and running.

@Chris I suppose that one aporove a vaccine, being confident that in a few years people won't start dying from it at a higher rate than they now die from coronavirus. If I seem stubborn, it is because I come from a quantitative field: I want to see the protocols and the numbers.

@Chris a friend of mine brought up a possibility that this is not possible simply because it is impossible, like saying that the sun wouldn't rise tomorrow. Perhaps, for people familiar with immunology/farmavology my question simply seems naive?

What protocols and numbers are you talking about? The protocol for the phase 3 trial? Can be found here. The published results from the phase 1/2/3 trials? All are linked at the bottom of this page.

You are correct that we have been creating and approving vaccines for a very long time, so the procedures for looking at efficacy and side effects of vaccines in general long-term are quite well developed. They occur via so-called "Phase IV" trials, also known as post-marketing surveillance.
However, one complicating factor with at least the Pfizer/BioNTech and Moderna vaccines is that they're the first mRNA vaccines ever approved. While I hope the companies have been following some of the volunteers from previous clinical studies of other mRNA vaccines, we're in somewhat uncharted territory right now. The vaccines appear to be safe and effective, at least on the scale of tens of thousands of Phase III test subjects, but we just don't know exactly how they'll behave long-term. They were approved in the US as "Emergency Use" products, meaning the upside of having them available outweighs any known or potential downsides at this point.
So, the technical answer to your question "how does one prove the long-term efficacy and absence of side effects in such a short time?" is that they can't prove it. Based on the available data to date, there's no reason to suspect that some previously-unobserved deleterious effect will become common, but we can't be 100% certain until the products have been in widespread use for years and possibly decades. However, given the seriousness of COVID-19 and its currently unchecked spread across much of the world, the benefits of having "highly, strongly, very most likely safe" vaccines (that are also very effective) are huge.

I will try here to sketch an answer starting from where @MattDMo left off.
Question:
How do we evaluate possible long-term side effects of a vaccine? (With specific application to the recently authorized vaccines for SARS-CoV-2).
Phase IV clinical trials
As @MattDMo has pointed out, the definitive answer can be given only in the Phase IV of the clinical trials, which is the follow-up of the vaccine/medication after its commercialization, which typically lasts throughout the lifetime of the medication. Obviously, such data are not available for the vaccines against SARS-CoV-2 (or any new vaccines). Thus, we have to rely on the information obtained in the earlier stages of the vaccine development. This leaves us with the following options:
Phase III of the clinical trials
Vaccine development process typically lasts 5-10 years, and the phase III of the clinical trials typically lasts about 6 months. Thus, typically one has the data for at least 6 months. This is however not the case for the vaccines against SARS-CoV-2, which were given emergency approvals after only 8 weeks of Phase III trials.
Animal models
Several years of vaccine development also allow for additional information: e.g., the vaccine could have been extensively tested on relevant animal models for extended periods of time. How one quantitatively estimates human risks from those for the animal model deserves a separate question, but the established animal model likely means decades of data avalable for comparing it with human. Again, this is not the case of SARS-CoV-2, which has been known for a bit more than a year, and for which no reliable animal model has been tested yet.
See this, this, and this articles for the general review of the use of animal models for vaccine development, and this one for the specifics of the animal models for COVID-19.
Similar viruses
In our case there are at least two very similar viruses that have been studied for years: SARS-CoV (first outbreak in 2003) and MERS-CoV (first outbreak in 2012). Although no vaccine has been available for either virus, much research effort has been put into this direction, and the data (at least on animal models) should exist. There might be even data for mRNA vaccines, which have been under development for some time already.
Nature of vaccines
Finally, the very nature of vaccination may explain why vaccines are approved faster than other types of medications, which can be for years in clinical trials. Adaptive immune system develops response to a new pathogen within about a week time. Thus, any adverse side effects are likely to appear during a week after vaccination, whereas the later developments have to do with the functioning of the immune system (other medications can have cumulative effects, if taken over a long period of time, or stay in the body for longer periods - such as medical implants). How one models quantitatively the long-term immune response is another question that deserves to be asked separately.
On this respect the new SARS-CoV-2 vaccines are taking a conservative approach, with the vaccines being counter-inducated to those with possibly different immune system responses: allergics, pregnant women, children.
Disclaimer
This answer could benefit from more reliable references, which I hope to pinpoint later. Also, it doesn't contain quantitative methods of risk estimation that I hoped for - rather it opens way to several more precise questions.

source: Stack Exchange

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

sort: votes


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AlphaFold: How do they determine the 100% accuracy threshold?
From what I read, it seems the current situation is like this: latest cutting-edge lab techniques get to an accuracy of around 90%. For example, they put a protein under an electron microscope or something, and from the images obtained they achieve a precision of 90%. Now Deepmind features an AI that has demonstrated in contests that it can also virtually fold proteins to 90% accuracy. Therefore, the problem is kind of solved.
Please correct me if my interpretation is wrong. But if it's correct, then a big question remains: how the hell can they know if a configuration is 100% true? Even the best technology can only reach 90%, so where do they get that 100% for comparison?

Just a guess - they could have created a synthetic protein where they know the exact sequence and used it as a reference?

Can you tell a bit more on the source which claims 90% precision of the laboratory methods of structural determination?

It seems I've made a mistake there. Lab results were actually set out as the 100 threshold, and Alphafold was compared against it. Because even lab techniques can have errors, they consider 90+ scores are about as good as 100.

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


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Coronavirus mutation: bad luck or a consequence of vaccination?
I would like to know whether a mutation within a virus (such as the new coronavirus mutation that appeared in England source) is a consequence of the vaccination program - maybe because it is stimulated to “fight against the vaccine”? Or whether it is just bad luck and the virus just happened to mutate during this vaccination time?
Additionally, if there any other historical evidence, can you cite examples?

A few (slightly pedantic points). The 'mutation' would never be a result of the vaccination program - mutation happen quasi-randomly. What you are suggesting is that the vaccination may cause selection on the mutation which may drive it to high frequency. Secondly, the virus doesn't 'fight against the vaccine'. The vaccine stimulates an immune response which causes the human body to more effectively fight the virus.

What vaccination programme? Almost nobody in Britain has been vaccinated yet! Or do you think the viruses heard about it on Twitter? Please do some homework before you post.

@user438383 thank you for your feedback. I sure did not know about this. Good to know the historical question has some relevance :D

@David I’m sorry if my OP offended you somehow. I did not know being curious would cause such a harm. And my supposition is that, even though the vaccination program just started, it is a coincidence like Chris mentioned. And if you believe there is no vaccination program yet... all good :)

I am not offended by your question, just trying to weed out questions that do not conform to our remit or standards. And I actually live in the country at issue and am aware of the state of our vaccination programme, whereas, you, from your US spelling, presumably are not and do not. As someone in the relatively high category 3, I still await my turn for the vaccine which there is every reason to believe  will be as effective against this strain as the one against which it was developed.

This is simply a coincidence. A RNA Virus will mutate all the time (although this one is pretty stable), there are thousands of known mutations (see Nextstrain for detailed information).

It is only a matter of time, until one of these will dominate the others. It may also be the effect of a few superspreading events where one virus type is strongly promoted, although it bears no or only a little effect over the other virus strains. Time and research will tell.
However, it is pretty much unlikely that one mutation in the spike protein (or even a few ones) will render the vaccine useless. The reason is twofold: First, the whole spike protein has a size between 180 and 200 kDa (source) meaning the protein has a lot of different epitopes against which antibodies can be directed. To render the vaccine useless, the whole protein had to be different.
This brings us to the second problem, because the spike protein is the protein which interacts with the target cell. If it would completely be changed, the virus would need a different receptor to interact with in order to enter the cell. Highly unlikely to happen, as the virus would need to "re-invent" it path of entry. As far as I know this has never been observed before.

Nobody has been vaccinated here yet! A few high-risk last week. Please do not accept invalid premises in bad questions.

As it has been pointed in the comments by @user438383, the mutation itself cannot be a consequence of the vaccination program - what is really suggested is that this is an escape mutation, i.e., adaptation that makes the virus viable in vaccinated persons.
However, there is no evidence (yet) that the new strain affects those who have been vaccinated - it well may be that these people are equally protected against this new strain. Moreover, chronologically the new mutation likely preceeds the vaccination campaign that has began only recently (even if it was detected/reported just after the beginning of the campaign).

Nobody has been vaccinated yet! A few high-risk last week. Please do not accept invalid premises in bad questions.

@David you seem to be misinformed. As of 3 days ago, 350,000 people in the UK have been vaccinated.

…out of a population of?


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What is an "open system" when it comes to PCR machines?
I have heard the term "open systems", such as here when it comes to RT-PCR machines, but I'm not 100% sure what this means, does this mean machines you can purchase yourself? Such as this one? ... compared to one that would be in a lab?
Also, I have heard that they come with the statement that they are for research purposes only and should not be used as a diagnostic tool, is this because anyone can buy them?

Based on the this paper it seems that the majority (if not all) real-time PCR assays are a closed-system when compared to conventional PCR and the primary reason for closed-systems appears to be to reduce contamination - all of this is detailed below:
Real-time PCR versus conventional PCR:

Real-time PCR testing platforms provide equivalent sensitivity and specificity as conventional PCR combined with Southern blot analysis. Since the nucleic acid amplification and detection steps are performed in the same closed vessel, the risk for release of amplified nucleic acids into the environment, and contamination of subsequent analyses, is negligent compared with conventional PCR methods.

Reduced risk of contamination:

The closed system for amplification and detection used with real-time PCR virtually eliminates the amplicon contamination caused by the opening and closing of reaction vessels which is problematic with conventional PCR and detection methods. Even with the closed system of real-time PCR, the laboratory may still choose to add uracil-N-glycosylase to the PCR mix for another level of amplicon contamination control.

...and:

The risk of contamination is considerably less with real-time PCR compared to conventional PCR, but still can occur (341). Since real-time PCR amplification is performed in a closed system, there is no need for individual air-controlled rooms as is recommended for conventional PCR. In our experience with real-time PCR, specimen to specimen contamination has become a greater challenge than amplified product contamination. The most obvious situation where specimen-to-specimen contamination can occur is with the transfer of specimen to the PCR vessel or to the DNA extraction tube. Care must be taken to avoid contamination of the pipette device with specimen and to avoid the creation of an aerosol by blowing out the specimen from the tip.

As for my secondary question about the "Research Use Only" statements I have observed; it is not entirely clear, but along with my original assumption, I also found the below:
This CDC page references some Real-time RT-PCR Primers and Probes that are for NOT FOR VIRAL TESTING USE and then goes on to say that:

Only primers and probes labeled for EUA use and distributed by the International Reagent Resource may be used for viral testing with the CDC 2019-nCoV Real-Time RT-PCR Diagnostic Panel.

So one reason is it could be to do with approval / red tape issues?
This seems to also be a possibility with other products:
https://www.diagnostictechnology.com.au/products/altona-realstar-sars-cov-2-rt-pcr-kit
https://www.sigmaaldrich.com/catalog/product/roche/tosrtro
One other possibility is that it's simply because they may be without a partnership with a medical laboratory:
https://johner-institute.com/articles/regulatory-affairs/and-more/coronavirus/

b) Research-only approach
Some manufacturers are considering selling their devices for “research
use only” without a partnership with a medical laboratory. Medical
laboratories could then use these reagents to offer a lab developed
test.
However, this approach should be viewed with skepticism, as the
“research only use” statement could be seen as a self-serving claim
that does not reflect the actual intended purpose: the product is for
diagnostic purposes.

In an open system, "mRNAs are detected because of their property of being expressed in the tissue sample isolated for study. This approach is in contrast to what are called closed-system approaches, in which the mRNAs to be detected are selected as candidates in advance of analysis; a contemporary example of a closed system would be a gene “chip” hybridization experiment." [Sutcliffe, J.G. (2001) J. Neurosci. 21:8306-9. “Open-System Approaches to Gene Expression in the CNS”] https://doi.org/10.1523/JNEUROSCI.21-21-08306.2001

Thanks, but I was more looking for an explanation about open-system vs closed system RT-PCR machines; and a bit more in detail with an explanation rather than just a quote.

If the question were about analyzing gene expression in general, this would be a good answer, but as the question is about qPCR machines in particular, this doesn't answer the question.


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

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

Found sources:

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

Please forgive me my English and any typos. :)

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

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


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Why does the DNA of Bacillus subtilis not contain DNA families of 20-37 members?
I am reading the book "Molecular biology of the Cell, 6th edition" and in chapter one page 18 the following figure is included

I am presuming this figure represents all genes within the Bacillus subtilis, which makes me wonder: why are there no families with 20-37 genes? There is a group for 4-19, and one for 38-77. What happened to all sizes in between?

You would need to read the original paper on which this figure is based. Do you have access to Nature? If not I can send you a reprint, but I don’t think this is a question about biology, but one of arbitrary data selection.

@David that may be the case, but to the OP that distinction cannot be easily known. So although an answer to this post might in fact point out arbitrary data selectivity as the cause, I think the question is otherwise biological in nature and therefore OK.

Based on the paper (open access) from which this figure was adapted, the 38-77 group consists of 5 gene families with 38, 47, 57, 64 or 77 members. In contrast, there are 284 “families” with 2 members, 91 with 3 members, 42 with 4 members, 25 with 5 members, etc. This is clearer in the original figure:

Thus the larger gene families are outliers and there simply exists no gene families in B. subtilis with 20-37 genes (at least by the methodology of this paper).

Very useful to see the original image and now that I know that there are also gaps within the groups given by my textbook the single gap between 19 and 38 seems a lot less extraordinary


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Can Taq polymerase be stored with PCR primers?
I don't think it's possible for TAQ to be stored with the primers, but I'm not sure. This storage wouldn't be long-term (a few days, or a week at most). Thoughts?

I have kept PCR stock solutions containing everything except DNA template for days to weeks at 4°C, and it works fine, at least for screening purposes (say, E. coli colony PCR or purified plasmid templates).

@gaspanic -20C would be ideal, though, especially for the dNTPs.

@MattDMo dNTPs are perfectly stable for months at 4°C, see for example here and here. I always keep an aliquot of my dNTP stock solution at 4°C both for convenience, but also to avoid repeated freeze-thaw cycles.

@gaspanic that's good to know, thanks

Yes, this is perfectly fine. Many companies sell PCR Master Mixes (granted, without primers):

Thermo Fisher
Sigma-Aldrich
BioRad
Promega
Qiagen

If you choose to make your own, make sure it's stored at -20°C, and be sure to aliquot it so it's not going to be subjected to multiple freeze/thaw cycles. Obviously you should mix it well before aliquoting, but even after thawing I would vortex it to make sure all of the components are well-mixed. Make a 2X master mix, and adjust to a final 1X concentration in the PCR tube with your DNA sample and nuclease-free H2O.


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What is the difference between mutation per base pair and mutation per genome?
Isn't genome size considered to be the number of base pairs present in DNA? So what is the difference between the mutation per base pair and mutation per genome? Are they similar or different?

I assume you read both terms somewhere?  Often, context supplies meaning. If you could directly quote the source of each term, you would likely get a good answer.

They are different normalizations of the same number. It's the question of whether you want to know how many mutations can be expected at a single position in a genome, or whether you want to know how many mutations occur across the entire genome.
See wikipedia, for instance:

There are several natural units of time for each of these rates, with rates being characterized either as mutations per base pair per cell division, per gene per generation, or per genome per generation.

Mutations per genome is the number of mutations per base pair times the number of base pairs in the genome (plus mutations that do not correspond to base pair substitutions, though they are usually ignored in these measurements).
E.g., $10^{-9}$ mutations per base pair in a genome of 3 billion base pairs correspond to $3$ mutations per genome.

not sure why this answer was downvoted/flagged. it's a pretty straightforward topic, not sure why a link is needed.


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What is the probability of virus undergoing a specific dangerous mutation?
Non-biologist here so apologies if the question is violating too many of the community standards for asking a question in the forum.
What got me thinking was imagining how much more terrifying the current situation would have been if the COVID virus had very long incubation period of something like 6 months and a higher mortality rate with the same rate of spread. By the time someone realizes that a virus is spreading, it would have already infected the entire planet. If it has a very high mortality rate as well, wouldn't that pretty much mean the end of the world?
My question is, what is the probability that this can happen? For example, what is the probability that a virus starts spreading with an incubation period and mortality rate of HIV but has the spread rate of COVID?

HIV and covid are two very different viruses, which behave diferently in how they are transmitted, and how they replicate themselves within cells. You may want to read this answer, to get a bit more background on how viruses lifestyles differ: https://biology.stackexchange.com/a/97324/59521

Thank you for the response, I understand your point about the HIV virus and how it's very different from the COVID one, and maybe I should have phrased my question differently, but my question was along the lines of, "what is the probability that a virus like the COVID virus mutating so that it has properties like a really long incubation time and more mortality rate"

Questions of probability are very hard to answer with any amount of confidence. I think a related question that is easier to answer may be: What are the viral traits that underlie measured variables like incubation time and mortality rate? Are there constraints imposed on the trade-off between these traits?

HIV and SARS-CoV-2 are two very different viruses in terms of how the are transmitted, how they replicate within the cells, how they interact with the immune system, etc. All of these aspects of a virus existence are highly adapted to assure virus survival (otherwise this virus quickly goes extinct). The ongoing mutations do help a virus to adapt to somewhat changing environment, but do not radically change it.
Thus, a virus that combines a long incubation period of HIV while being highly contagious as SARS-CoV-2, would be a completely new species, different from either of these two viruses in its genetic makeup, lifestyle, etc. It could take millions of years of evolution for such species to develop. Moreover, such a development is unlikely, since such a virus would exterminate its host, thus becoming extinct itself. The scenario that is more plausible is that of Ebola - a virus that exists as relatively harmless in some animals, and can evolve within them, but is highly lethal when it spills to humans, which results in deadly out breaks that quickly end. Probability of such a nightmare scenario is as small as a probability of the world ending due to a black hole generated in Big Hadron Collider or huge meteorite striking the Earth - while it cannot be mathematically excluded, it is too small to account for it in our daily lives (as compared to other dangers).

That's good to know. Thanks for the explanation. I can sleep a bit better at night.


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Why are there 10 base pair steps, not 16?
In a biochemistry course I'm taking, the lecturer emphasised that there are 10 possible base pair steps; I've included a screenshot of a slide stating this. This confuses me, because I cannot work out why it's not 16; why are the 6 greyed out in the image not allowed (for example, CG stacked on CG counts, but GC stacked on GC doesn't)? TA|AT is listed as distinct from AT|TA, so it's not that the greyed ones are redundant.
I've found a couple of papers mentioning that there are 10 base steps, but not why. (I can't get hold of the lecturer.)
Thanks in advance!

CG stacked on CG and GC stacked on GC are the same step with the chain turned by $180^\circ$, so there is no need to count it (and other similar steps) twice.

@Vadim, would you mind expanding your comment as an answer?

Unlike RNA, where the sense of the molecule is unique, DNA is double stranded, with the two strands having the opposite sense. In the sense of chemical stability it odesn't matter, which sense is considered positive, and which is negative.
Thus, if we consider a base pair step WX|YZ, we have Y folowing W on the positive sense strand (W->Y), and X following Z in the negative sense (antisense) strand (Z -> X). This means that, if we labeled the strands differently, we would have Z->X on the positive strand and W->Y on the negative one, i.e., we would have base pair step ZY|XW. I.e., the general symmetry rule is
$$
WX|YZ \rightarrow ZY|XW
$$
In particular, this means that CG|CG is identical with GC|GC, whereas TA|AT is identical with itself, rather than with AT|TA.
Visually, this symmetries are obtained by rotating the image of the base pair step by 180 degrees, as can be readily seen in the image provided in the question.

Maybe worth pointing out that OPs own image demonstrates why there is 10. It shows the 16 'possibilities' and grays out those that are duplicate via rotation. With the picture in hand you can just... count.


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

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

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

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

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

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


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Is it plausible that strict lockdowns made it more likely for the new variant of COVID to have emerged?
My idea is that strict lockdowns put greater evolutionary pressure on the coronavirus by restricting oppurtunities to be transmitted, meaning that a faster-spreading variant had much less competition.
Is this at all plausible? Was it just as likely for a faster-spreading variant to become the predominant one without lockdowns?

It's actually a complicated trade-off between the total amount of time that the virus has time to mutate and number of hosts it can mutate in. You've basically selected the wrong answer. aliential's answer links to a paper that does this sort of (non-trivial) analysis. I'll also note there that it's much harder to quantify the chance that rare "human lab" events can occur, which are thought to be at the origin of the latest UK variant of concern. https://virological.org/t/preliminary-genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations

Okay, I guess that I am not going to select an answer, as I am not really qualified to judge. That answer made sense to me at the time.

@kCODINGeroo Why do you ask a question if you aren't qualified to accept an answer? Only you as the original poster can accept an answer.

While I get your intuition, the hypothesis seems implausible

Emerge of new CoV variants should be considered proportional to the
current spread of the virus. Each virus has a certain mutation rate that surely does not depend on lock-downs.
It seems implausible to interpret
lock-downs as physical limitations to viral spread, that could potentially be
overcome by any mutation.
Even if CoV magically learned to
teleport to different households, such an ability would always represent immense advantages; an advantage that does not need lock-downs to be effective
Lastly, the differential viral competition is neglectable so far; we are at 6 of 100 thousand infected persons. So basically a 0% chance that a virus would infect a person who has acquired an immunity due to a previous CoV infection. In your model this person, who is immune, further would need to NOT be immune because quarantine prevented the (previous) infection.

This is more plausible (second point below) and less plausible (third point below).

Selective advantage The emergence of a new strain of a virus relates to the selective advantage (Gordo 2009). This selective advantage might be that the reproduction rate is relatively higher.

Reproduction rate The selective advantage (in terms of relative growth rate) is based on the relative growth rate of the virus. Because the growth rate for viruses is not directly proportional to the reproduction rate (Wallinga 2009), this means that better selective advantage is not exactly the same as better reproduction rate (and that is just the selective advantage due to reproduction rate). Instead, it is more like related to the reproduction rate minus one. The relative (initial) growth rate of the mutated virus (made dimensionless by multiplying with generation time) gives the relative growth factor  $$\text{growthrate} \times \text{generation time}  = \overbrace{s}^{\text{selective advantage}} = R_{mutant}- R_{other}$$ If you have some mutation that gives an improved effective reproduction factor $R_{mutant}/R_{other} = c$ then the difference $R_{mutant}- R_{other}$ will be larger for a larger $R_{other}$. This is not the case with a lockdown ($R$ will be typically lower) and in a situation with a specific ratio $R_{mutant}/R_{other} = c$ the relative growth of the mutant will be smaller if $R_{other}$ is lower

What makes reproduction rate higher? There is a small catch with this second point (from which you could conclude that growth of new strains is higher without lockdowns). Another non-linearity is that the reproduction rate is not scaling linearly with the infectivity of the virus.
For instance Ferrari et.al. (2006) model the probability of infection as an exponential function of the rate of transmission

The susceptible nodes become infected in the next time-step with binomial probability 1−exp(−βI), where β is the rate of transmission across an edge, and I is the number of infected nodes to which the individual is connected.

The infections are a function of time and proximity (and also the susceptibility and infectiousness of people), and this is not homogeneously distributed. This makes that a simple reduction of 'infectivity' by half is not at the same time also making the effective reproduction rate become halved.
You could see the reproduction number being buffered in some sense. There is an excess/overflow of transmission in some parts of the network. When you are sick, then most likely your family members are gonna get sick as well. When the virus becomes half less transmissible, then it is not like only half your family members are gonna get sick. Reducing the transmissibility might have an effect for short-term contacts (which are important pathways as well), but it is of less influence for intensive contacts.
This buffering makes that the transmissibility of the virus (the reproduction rate) is not so much controlled by the changes in the properties of the virus. The transmission is more controlled by the human traffic and contact network (and the fluctuations occurring within this network/traffic). If an average person sees, on average, only 3 people within the infectious period, then the basic reproduction number will be at most 3 and it can't suddenly make a big jump. You can not infect more than 3 people if you do not see more than 3 people, so the virus can become more transmissible but it won't influence the reproduction rate 'as much' (unless there is an entirely different mode of transport). (I am putting stress on 'as much' because there will be some influence, just like adding acid to a buffer will not have zero effect, but it just won't be the same)
Any growth of small mutations in new strains is (initially) more likely to be occurring randomly. Viruses mutate a lot, and there will a lot of probability that there is a lucky sample (many others will be unlucky) that might accidentally reach some area with a fast growth rate and with little competition (isolation from competition is a good, but also likely, route for a non-competitive mutation to grow in number). This randomness becomes larger when the total numbers are smaller. If a new strain hits a (relatively) clean area then it will spread out without any/much competition and it can become big (especially if it is an area without much control) and spread over a large area unnoticed.
This isolation might be more likely in a scenario with strict lockdowns, which makes the spread of the virus more chaotic (it's like rolling a dice a few times, you'll be more likely to get the same number with a high frequency in comparison to rolling the dice often; the lockdowns make the spread dependent on fewer dice rolls and give more chances to some mutation to slip through, reach some prosperous less lock downed area, and become more dominant)

So, in general there is no clear influence from a lockdown. In general the emergence of new variants relates to Fisher's fundamental theorem of natural selection

"The rate of increase in fitness of any organism at any time is equal to its genetic variance in fitness at that time."

The second point above (lower fitness/growth-rate results in lower natural selection) relates to the fact that it we reduce the fitness with a factor $c<1$ by a lockdown, than the variance of the fitness changes by a factor $c^2$. The change of the fitness will scale with $c^2$ and the relative change of the fitness will change with $c$.
The third point above relates to a breaking of the assumptions (there's no homogeneous spread of the virus). Breakdowns can create relatively separate/isolated regions and the spread may not be via a Malthusian growth model but instead more chaotic (with random branches like a thunder bolt). This makes it not unthinkable that a variant emerges quickly by a random effect and without much difference in selective advantage.
Some references

Gordo, Isabel, et al. "Genetic diversity in the SIR model of pathogen evolution." PloS one 4.3 (2009): e4876.

Wallinga, Jacco, and Marc Lipsitch. "How generation intervals shape the relationship between growth rates and reproductive numbers." Proceedings of the Royal Society B: Biological Sciences 274.1609 (2007): 599-604.

Ferrari, Matthew J., et al. "Network frailty and the geometry of herd immunity." Proceedings of the Royal Society B: Biological Sciences 273.1602 (2006): 2743-2748.

Current Biology 30, R841–R870, August 3, 2020 R857, does support some of your theory.
The paper summarizes the scientific basis of their statements:

Even though the adaptive significance of genetic variants remains to
be established, we can use evolutionary theory to gain insights about
how natural selection might act on disease characteristics.

The mutation rate is related to the population size which has stayed nearly as high this winter as it was with dense crowds previously, regardless of distancing, so the following statement is all the more likely,

some mutations may become more strongly selected in the presence of
social distancing if they allow for viral transmission despite the
intervention (for example, mutations affecting aerosolization or
persistence in the environment).

i.e. physical distancing will select for better breach of distancing, and quarantineing will select for higher transmission during the asymptomatic days prior to fever.
The transmission methods aren't very well know, i.e. asymptomatic transission, transmission by children, peak transmission before symptoms appear, rates of contact Vs airborn transmission.
So, you are right, distancing encourages mutants that reproduce and transmit despite distancing tactics.

Do lockdowns help new mutations emerge? - No.
Mutations appear at an approximately constant rate in every genome replucation event. In this sense, the lockdowns reduced the overall number of mutations, by reducing the number of infections and new replucation events.
Could lockdowns help new mutations become prevalent? - Possibly. Whether a new mutation survives and becomes widespread depends on its fitness, vis-à-vis the adverse environment in which the virus exists. The more contagious viral strain has a selective advantage over the other strains. The speed with which such a strain pushes out the other strains out of the existence, i.e., the time that it needs to fix in the population, depends on the effective population size. In this respect, lockdown resulted in reducing the effective population size, which could have resulted in faster fixation of the more contagious strain. (It is important to keep in mind that the lockdown wasn't waterproof - the virus was still spreading, although at a lower pace.)
In other words, the lockdown could have acted as an evolutionary bottleneck, reducing the viral diversity at the expense of the less fit strains.
Has this really happened? - No. We are not dealing with this situation, but rather with a viral strain that has emerged only recently, which is certainly far from having fixed in the population. One cannot even be sure that it has a selective advantage - it is more contagious, but may have other, yet unknown, shortcomings.
If the new strain does have selective advantage, the future lockdowns might "help" it to become the dominant strain. This shows that lockdowns are not sufficient to eradicate a virus  - as opposed to completely quarantining/isolating whole groups of population, as was done in China or during the Ebola outbreaks. Eradicating the virus however never was the point of the lockdowns: they were implemented to slow down its spread, so that it does not overwhelm healthcare systems, so that effective testing procedures could be put in place, and to allow time for developing vaccines.

Your first answer on "Do lockdowns help new mutations to emerge" assumes that the spread can be stopped by the NPIs. If, however, the spread can't be stopped, but only limited, it's my understanding that it will help new mutations to emerge. Furthermore, NPIs apart from complete isolation, can introduce strains that are more transmissible, as they're the only ones that will survive

@Highmastdon I didn't make such a strong claim - I meant that the lockdowns reduce the basic reproduction rate, which means less infectioned eprsons and consequently less replication events for virus... for a period of time - if no other measures are taken, the eventual  number of the reproduction events may be just as high, although the effective population size still remains lower.

You are the victim of the "post hoc ergo propter hoc" fallacy: just because event B follows event A doesn't mean that B is caused by A. The probability of a mutation to occur depends on the number of virions out there multiplied with some constant that models the faithfulness of the virus reproduction machinery. The lock-down was instituted because the number of infected persons - and hence virions - was high. Thus, both the lock-down and the occurrence of mutations share the same cause, one of the possible reasons for nonsense correlations.

I don't think the question makes any claims (and thus commits a fallacy) - it is more an inquiry about a possible relation between two events. Also, emergence of a new strain depends not only on the availability of mutations, but also on the evolutionary pressures, the random drift, the population structure - all of which were affected by a lockdown.

The OP - whether formulated as question or as statement -  contains a hypothesis. This hypothesis is based on a nonsense correlation. And the probability of a mutation arising depends on the factors I mentioned; the factors you named determine whether this mutation can spread.

the OP is asking about the emergence and spread of the new strsin, not just about a mutation. In fact, they even do not mention mutations.


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PCR and large-scale PCR
I have performed PCR with 50 μL, which showed a clear band in the gel electrophoresis. I then performed large-scale PCR with 3650 μL, which showed an unclear band in the gel electrophoresis. What can be reason for this? Could it be plasmid loss even though there is a band, just a very unclear one? It should be mentioned that the single PCR was performed in the summer, and the large-scale was performed now

It could be poor mixing of the reagents, poor thermocycling of the larger volume, or a host of other issues.  More details on how both experiments were conducted would be useful. Is the 3.6 mL reaction in a single tube? How are you cycling a volume that large (separate water baths)? Did you increase the length of your steps to account for slower temperature change of the larger volume?

@acvill thank you. I made the large-scale in a falcon tube and then moved the mixture to PCR tubes each containing 50 μL, so the PCR conditions should be the same as the single PCR amplification

Still the question is: Did you mix really well?

Do you have photos of your gels?

I made the large-scale in a falcon tube and then moved the mixture to PCR tubes each containing 50 μL, so the PCR conditions should be the same as the single PCR amplification

If all reagent concentrations and cycling conditions are the same, I suspect that you did not sufficiently mix your large-volume reaction prior to dispensing as 50 μL aliquots.

It should be mentioned that the single PCR was performed in the summer, and the large-scale was performed now

If you were using the same polymerase and primer stocks for the small- and large-volume reactions, were the stocks properly stored in the interim? Recombinant DNA polymerases in glycerol buffers have shelf lives of months to years depending on the supplier specifications and storage conditions, though you should expect some decreased activity after several months.


text:
What makes some viruses more infectious than others?
This week a new strain of the SARS-CoV-2 virus was discovered in the UK, and reports are saying that it's more infectious than the strains we've been dealing with for the past year. Which made me wonder: what is it about different strains (or different viruses in general) that makes them more of less infectious than others?
They've been saying that they don't think the new strain will be any more resistant to the vaccines. Does that mean they're no more able to evade the immune system? Or is it just the immune system that hasn't been primed by a vaccine?

To name a few parameters that can determine the infectiousness of a pathogen:

Transmission pathways used (aerosols, surfaces, vector organisms, feces etc.)
Molecular affinity to bind to host cell (how well does it penetrate the cell)
Strategy within host cell (lysogeny, lysis)
Interaction with the host’s immune system


text:
What type of bug is this?
Found two larva/eggs in a suitcase. The egg/larva were around same size or maybe little bigger than a grain of rice. When I put them on counter top to better examine, one hatched and a SINGLE insect popped out! It was fast moving when hatched and kept cleaning its legs. It was maybe the size of a grain of rice. I personally was thinking cockroach but it was a single insect from egg/larva!?!? Is it a bed bug or something else??? (We reside in Alabama.)
https://share.icloud.com/photos/0mQiO0JfeRwR3z7duvPSthrZw

If you have the photo on your device, use the mountain symbol to put the photo directly in your question

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible) — photos must be uploaded (not links); 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information; and 4) an estimate of the size of the organism. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Thanks!

In addition, there is an excellent post with information about bed bugs already on this site. If that is your primary concern please search on this site for "bed bug" and then delete this duplicate post if that answers your question.

I edited post as instructed. And also searched “bed bug” as instructed  Still left with question... Any advice on bug type? Comments? Please help...

From the evidence at hand, we can say Order Diptera (two-winged flies) with certainty; the suborder Brachycera seems more likely (the antennae of the adult in closeup are very short; Nematoceran flies usually would have antennae at least as long as the head is wide [those that don't bear NO resemblance to the OP photo]); beyond that, there are too many good possibilities (members of the family Drosophilidae [the geneticist's "fruit fly"] being just one of many possible groups).


text:
What mammals can rotate and move their ears the most?
I found out that rabbits can rotate their ears 270 degrees, and also move them up, down and independently. Are there any other mammals that can control their ears' position that well, or even better?

Can't find a study with actual measurements, but from personal experience horses can move their ears through a pretty wide range: tilting about 180 degrees forward & back, and rotating independently about the same angle.


text:
Difference between diffusion and osmosis
Osmosis in plants so called diffusion too. Need to understand the difference between osmosis and diffusion Because this both process transport molecules from region of higher concentration to region of lower concentration.

See in diffusion co2 o2 gets transported from high concentration to low concentration through semi permeable membrane and And in osomosis also water gets transported from high concentration to low concentration through semi permeable membrane

Does this answer your question? When does DIFFUSION occur and not OSMOSIS, and the otherwise?

Because this both process transport molecules from region of higher concentration to region of lower concentration.

This is not strictly true. Molecules don't move in the same direction, rather the concentration moves towards equilibrium (higher to lower)
In Osmosis, the first characteristic is a semi permeable membrane. (More on such membranes in College level biology). Secondly, it is the solvent molecules that move, so that concentration is made equal on both sides of the membrane.

This is the most important feature in osmosis. Solvent molecules move, from a region of low concentration to higher concentration. When solvent molecules increase in a region of higher concentration (right side in the image), the concentration comes down; while that in the region of lower concentration (left side in the image), increases.
On the other hand, diffusion is the movement of the solute molecules. If you were to spray a perfume in one corner of a room, the smell would then be felt everywhere else. This is because the perfume molecules are diffusing through the room.

In a different example, suppose you have a box with a partition, full of gas. One side of the partition has the gas at high pressure and the other side has a low pressure. When you remove the partition, molecules of the gas will diffuse from the side with higher concentration to the side with lower concentration.
In summary, the difference between osmosis and diffusion can be found in identifying WHICH molecules move.


text:
When was peptidoglycan discovered?
I've searched for some time now, but I can't find a definitive answer. The closest I have gotten is "knowledge about peptidoglycan structures dates back to the 1970s–80s" from this paper.

This is a not really a good question for this site — and if you ask better questions please put them in the question rather than the assume we remember the title. The reasons are 1. The purpose of this site is not to construct a chronology of the discovery of every biological compound, 2. Nobody on this site knows the answer to that sort of question without doing a search, 3. You can easily find it yourself — search “dictionary peptidoglycan” — and choose a reputable primary dictionary from the results. I chose Merriam Webster and it gave me 1966. For a citation you might need to look further.

@David not sure what your qualm is with the question. If people have this question, they can look at it, otherwise they can just as easily not open this thread. This site even provides a history tag, so it seems that this falls within the meta. Additionally, Merriam Webster does give 1966 but it’s very vague and unconvincing (and I had looked at this before posting). I asked simply because the answer seemed complicated, and would probably be best answered by someone with knowledge of the topic.

First, tags do not define what's on topic and whether a question is satisfactorily presented. That is explained in the [Tour] and the Help. (Not sure what you mean by "falls within the meta".) There are circumstances where a question about the history of biology is on topic, but, as is clear from the Help on Asking Questions you need to make it generally relevant and provide context. As you had not done this I explained how to find the answer. The aim of the site is to build a library of questions about biology that are of general use.

https://pubs.acs.org/doi/pdf/10.1021/bi00879a016?casa_token=L-dTOhCAdyUAAAAA%3AMkJotlvSnQXk9gL1gkdl7DkOgSi25bNmMWO-OOxffK3qFFEo_mdXfmRHOk4PbItEf5ZYnIa7N5mtISw&

The discovery of peptidoglycan, as present in the bacterium cell wall took many years.
“The terms mucopeptide, glycopeptide, or murein, used by some authors, are all synonymous with peptidoglycan.” [Ghuysen, J.M. (1968) Bacteriol. Rev. 32:425-64] Among those, Weidel and Pelzer previously coined the term murein [Weidel, W. and Pelzer, H. (1964) Adv. Enzymol. Rel. Areas Mol. Biol. 26:193].
Regarding the organized, higher structure of the peptidoglycan as found in the Gram-negative cell envelope, Salton [Salton, M.R.J. (1994) New Compr. Biochem. 27:1-22] mentioned the following:
“The exact nature of comparable ‘wall’ fractions obtained from Gram-negative bacteria remained a matter of uncertainty until the advent of electron microscopy of ultra-thin sections of bacterial cells as demonstrated by Ryter and Kellenberger [Ryter, A. and Kellenberger, E. (1958) J. Biophys. Biochem. Cytol. 4:671-678.]. The response of cells to the Gram stain procedure and the early chemical analysis of ‘cell wall’ preparations clearly pointed to some basic differences in the properties of the envelopes of Gram-positive and Gram-negative bacteria and the greater chemical complexity of the isolated fractions from the latter organisms [Salton, M.R.J. (1953) Biochim. Biophys. Acta 10:512-523.]. The structural complexity of the Gram-negative cell envelope was clearly resolved in the thin sections of Ryter and Kellenberger [Ryter, A. and Kellenberger, E. (1958) J. Biophys. Biochem. Cytol. 4:671-678.] and established the presence of an outer membrane as a characteristic feature of the cell envelope. The mysteries of the structure of the Gram-negative cell envelope were finally solved with the demonstration of the thin layer (peptidoglycan) between the outer and inner (cytoplasmic) membranes by use of lanthanum-stained thin sections by Murray et al. [Murray, R.G.E. et al. (1965) Can. J. Microbiol. 11:547-560.], and the isolation and demonstration of the thin murein sacculus of E. coli by Weidel et al. [Weidel, W. et al. (1960) J. Gen. Microbiol. 22:158-166.]. Thus, the complex cell envelopes of Gram-negative bacteria were resolved as consisting of an outer membrane anchored to the underlying rigid, thin, peptidoglycan layer or sacculus.”


text:
Inheritance of FEVR (Genetic Disease)
If a woman has FEVR and is affected by the disease, what are the chances of her passing the disease to future generations. I read somewhere from a credible source like NIH(I couldn't find the link again, I am attaching another https://rarediseases.info.nih.gov/diseases/1613/familial-exudative-vitreoretinopathy#:~:text=Familial%20exudative%20vitreoretinopathy%20(FEVR)%20is,the%20blood%20supply%20to%20retina.), that the babies that the woman conceives could be affected by or carrying the FEVR causing genes, or may neither be carrying nor affected by them. Depending on the type of inheritance, which are autosomal dominant, autosomal recessive, or X-linked recessive, the chances of having a normal baby vary. The chances of having a healthy kid for autosomal dominant and autosomal recessive are 50% and 25%, respectively ( I am intentionally excluding the possibility of X-linked recession).
Therefore, if the inheritance is autosomal dominant, then, there is a 50% chance that the baby is healthy and not carrying the genes. And the successive generations created by the baby will not have the gene causing FEVR. Is my understanding correct?

Are you asking about the mendelian inheritance calculations?

The answer depends on (at least):

whether the woman is affected by the condition
whether the allele is autosomal dominant or autosomal recessive (excluding X-linked recession)
the frequency of the diseased alleles in the population
the presence or not of inbreeding

Below I assume no inbreeding.

The woman is affected and the inheritance is autosomal recessive. This means that the woman carries two disieased alleles and with certainty passes one of them to her children (i.e., with probability $1$). Whether the children will be affected by the condition depends on whether they get a second diseased allele from the other parent. Assuming that the frequency of the diseased allele in the population is $p$, this means that the probability of a child inheriting the disease is $p$.
The woman is not affected and the inheritance is autosomal recessive. The woman carries only one diseased allele, and passes it with probability $1/2$ to her child. The probability that a child is affected, i.e. that s/he has two diseased alleles is $p/2$.
The woman is not affected and the inheritance is autosomal dominant. In this case the woman carries no diseased allele, so the children are not affected.
The woman is affected and the inheritance is autosomal dominant. The woman carries at least one diseased allele, and could be carrying the second with probability $p$. In the former case she passes it to her child with probability $1/2$, in the latter with probability $1$, so the probability that the child inherits the diseased allele is $1/2 + p$. This is also the probability that the child is affected by the condition, since they will be affected regardless of the allele passed by the other parent.

Assuming very small probability $p$, case 4 gives us the probability $50%$, whereas the probabily in cases 1 and 2 is much lower. The numbers given in the question are calculated assuming Mendelian experiments, which are a heavy case of inbreeding (and even then not quite correct).
John H.Gellespie, Population genetics
Matthew Hamilton, Population genetics

The above assumes complete penetrance; many disease show only partial penetrance, where some individuals who carry the disease allele(s) show no sign of disease. That greatly complicates calculations, significantly changing cases 2 and 3 above.


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Is amphibians being descended from fish reflected in the animalia taxonomy?
I think it is common knowledge that amphibians are descended from fish. At some point there was a transition from sea to land.
But when I try to confirm this through the Animalia taxonomy, the scientific classification of fish goes

https://en.wikipedia.org/wiki/Fish
while the scientific classification of amphibians go

https://en.wikipedia.org/wiki/Amphibian
If we draw this as a tree of sorts, we end up with

it seems to be quite obvious that fish and amphibians belong to the same phylum but different clades, but I'm not sure how that proves that amphibians are directly descended from fish?
I'm interested in a tree that shows amphibians branching off of the fish lineage.

Look in to the difference between cladistics and phenetics/phylogenetic trees.

the phylogenetic trees i found only went as far as animalia, if were looking for fish or amphibians. so i was hoping cladistics would be like another focused phylogenetic approximation of the animalia kingdom, are they not related?

They are related but not the same. If you read about them it's easy to find comparisons of how they differ.

Your "tree" is drawn incorrectly. What you have labeled as ancestors and descendants are nested groups. Vertebrates and amphibians are both chordates, and amphibians are also vertebrates. The wikipedia taxonomy box uses outdated, non-phylogenetic terminology.

Fish are a paraphyletic group: that is, any clade containing all fish also contains the tetrapods, which are not fish. For this reason, groups such as the class Pisces seen in older reference works are no longer used in formal classifications.

You got something completely wrong. In evolution one can not say that one taxonomical group evolved from the other. We say that two taxonomical groups have common distant relative. With that said all vertebrates have common distant relatives. Important is to know when did the branching in speciation happened.
Proto-amphibians evolved in Devonian by further speciation from relative that was sarcopterygiian (fish). It was a fish with some properties of amphibians (lungs and bones in appendages).

From:
https://en.m.wikipedia.org/wiki/Rhipidistia

Can you please put a source for your quote and the phylogenetic tree?

are you trying to say that all amphibians are fish but not all fish are amphibians? If that is true I don't understand how you cannot logically conclude that amphibians have to have evolved from fish, without making any inferences about intermediate transitory forms?

"The first major groups of amphibians developed in the Devonian period, around 370 million years ago, from lobe-finned fish which were similar to the modern coelacanth and lungfish." <- this is the language from wikipedia that led me to believe amphibians evolved from fish

@notacorn Yes, what you said is exactly how it works. Amphibians, as well as reptiles, mammals, and birds, are technically a type of highly modified fish. They don't stop being fish just because they are highly modified from the ancestral form. Some fishes, such as lungfish and coelocanths, are more closely related to amphibians and reptiles than they are to sharks, bass, or other fishes.

@notacorn I think that Domagoj's point is that "fish" is not a very useful grouping in the first place. "lobe-finned fish" is a slightly more useful classification, as it's much more specific.

Maximillian is correct "fish" is a not a useful term, it is polyphyletic by most usages, the closest useful term would be vertebrata

Check through the classification of lungfush:
under a cladistic view, tetrapods are themselves considered a group within Sarcopterygii
https://en.m.wikipedia.org/wiki/Sarcopterygii
And
https://en.m.wikipedia.org/wiki/Rhipidistia


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Are animal cells animals themselves?
If all life can be divided into several kingdoms, and if the cells that make up organisms are the smallest units of life, does that mean that cells are part of those kingdoms as well? E.g. are animal cells classified as animals themselves too?

This is like asking if your arm is considered an animal. No, (like the cell), it's a sub-organismal part of the animal. Recognize that our classification systems (which are arbitrary ways of trying to conceptually organize a continuum of genetic diversity) organize genetic diversity at the organismal level. I feel like this is sort of related to the fallacy of division. I think you'd also benefit by reviewing the criteria to be an animal.

Also, If an animal cell was capable of living as a unicellular organism, I would posit that either the cell or the organism as a whole may get reclassified.

Eukariotes are more logically defined as unified multicellular groups in science.
You are right that Eukariote cells share many traits with unicellular organisms, like meiosis division, cell walls, inner metabolism, and it is an intelligent view to consider them as related to unicellular organisms in most ways, although your proposition is mostly of comparative and philosophical us, rather than a scientific biological reasoning and description.
Animal cells share the same chromosomes, which is different from species of micro-organisms, so that eukariote stem cells can differentiate into the specialized cells. Most species definitions contain a strong reproduction framework which applies to all species whereas Eukariote cells start from zygotes and then communicate with each other with signalling hormones to form a specific superstructure which are used to produce more zygotes, which contrasts with procariote definitions of a species.

So far as I know (per https://www.genetics.org/content/181/1/3 ) meiosis evolved early in the history of the eukaryotic lineage.  Also, there is no direct connection between multicellularity, hence zygote formation, and the domains of life - so far as I know, eukaryotes simply happened to be the ones that developed it.

I didn't upvote your answer because i agree with it, just because it showed some effort and contained some accuracies. I said that animals are defined by reproduction type, i.e. multicellular animals reproduce as indivisible groups, typically through zygotes. animals can be a colony which has arms and legs and nerves stemming from the brain to the toes, so they are considered as a unified multicellular groups, because it simplifies useful communication.

My opinion is yes, but note this could be subject to debate.  This is a semantic question and someone could decide arbitrarily the other way, but I'm not aware of a formal counterargument, and logic seems to demand it...
Consider Devil facial tumor disease.  I've linked a Wikipedia article there, and Wikipedia usually is very good about providing taxonomy for organisms and it's a shame they didn't do it here, as they are experts in semantics.  NCBI also does not provide a taxonomy.  But logically, if we were going to provide one, how could we possibly categorize those cells?  They are living, they reproduce, they evolve, they are eukaryotes, and based on their DNA ... they are animals!
A less clear-cut instance leading in this direction can be seen with Sacculina carcini, a parasitic barnacle of crabs.  That does have a multicellular larva, but it is not a very typical mollusc, and it illustrates that it is the cells and descent of an animal, not its form, which determine its status.
Based on these things, I would say an animal cell can potentially survive, thrive, and in reproducing itself, become recognized as an organism despite its form.  However, there is a contrary semantics to be considered, notably in the case of the HeLa cell line.  In that instance, in part due to the genetic instability of the tumor cells and their dependence on human intervention, a proposal to name them as a species did not gain traction, while I believe some argued with an eye to legal issues that the cells were still essentially part of the individual Henrietta Lacks.  However, in nature the definition of an individual can be fluid - in polyembryony one individual can divide into many, and even in humans one individual can become identical twins, so I wouldn't say that an isolated cell must remain part of the parent individual.  Meanwhile, cells of different genetic origins can join into "a" slime mold, though they usually sort themselves out by species.  In that instance we have a clear precedent of deciding the taxonomy of individual cells of an organism ... but it's not an animal.
Love it or hate it, biology will do whatever it can, without regard for how we choose to think about it.


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Is there any difference between strain and mutation/mutant?

Experts are closely monitoring the strain, which has rapidly spread
through the country's south.

Source
Most of the media/newspapers are calling VOC-202012/01 a COVID strain, instead of a COVID mutation/mutant.
Is there any difference between strain and mutation?

You can think of "strain" roughly analogous to how you would think of "breed" in the context of dogs or horses.
There might be some key mutation that identifies members of a strain over non-members, but you would expect to find other genetic differences as well. "Strain" for a virus is not referring to a particular mutation but to the viruses on one side of some fork in their evolutionary history.

As @BryanKrause has correctly pointed out, strains for viruses and bacteria are the same as breeds/races for mammals and birds - the differences between strains are sufficiently small that they cannot be considered different species, yet they may differ by more than one mutation.
Strain is a somewhat generic term, whereas more refined terminology may exist for every particular virus. For example, in case of HIV one distinguishes types of virus (HIV-1, HIV-2, SIV), the groups within each type, and the subgroups. Depending on the context any level of this taxonomic division can be referred to as "strain".
What further makes distinguishing strains difficult is that breeds/races are usually defined by having different phenotypes. The phenotypical differences between different viral strains are more difficult to define, so it is not uncommon to distinguish different strains (or even species, as in the case of flaviviruses) simply by the number of mutations or the fraction of nucleotide differences between sequences.


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Does anybody know what kind of tree is this?
I saw this tree yesterday and I liked it. It is around 1.5 m. I did some search on internet and thought it might be Holly, but I'm not an expert on trees. So I wanted to ask you, does anyone know what kind of tree is this?
Location:The Netherlands

Looks like a holly, similar to English holly ( at least that is that it is called in the US ) .There are different cultivars . It has been pruned to a tree shape .

Thank you for the answer.


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Questions regarding transformation in bacterial cells
First off, in transformation the donor DNA aligns itself with the complementary bases in the recipient DNA.
Now a "perfect" alignment of the donor DNA ( Sorry if my terminologies are incorrect ) would mean that an exact replica of the donor DNA fragment already exists in the recipient DNA. If such is the case no genetic recombination will take place but genetic recombination is observed, this is the part where I get confused.
If the DNA fragment is aligning itself with the donor DNA and and causing a genetic recombination, then obviously the donor DNA fragment should contain some variation from the recipient's DNA. This would mean that the alignment of the DNA fragment isn't perfect and not every base in DNA fragment can form a complementary base pairs with the recipient DNA. ( Again sorry for usage of improper terminology as I'm a new student who just started an introductory course pertaining to microbiology ).
Now the problem is -

Shouldn't it be energetically unfavorable for the donor DNA fragment to replace the original DNA as the original one should be able to form complementary base pairs with the entirety of the recipient DNA while the donor DNA can do so only with a part of the recipient DNA.
After thinking about this, I thought of an assumption to explain this. The RecA protein involved in transformation is somehow forcing this process to happen. The thing is how? I have zero knowledge of enzyme chemistry and can't understand how this could possibly happen?
So is this assumption correct? If so is there any reference material explaining how RecA protein could be doing this?

This brings me to the second issue. This newly created DNA should now have many irregularities, how are they fixed?
After some thinking, I came to the conclusion that as RecA proteins are involved in DNA repair, the RecA protein simply fixes the irregularities. Is this line of thinking correct?

In short, I have assumed that a RecA protein is causing a DNA fragment which can not form complementary base pairs with the entirety of recipient DNA to be accepted in the recipient DNA, following which the irregularities that arise are also fixed by RecA. Is this line of thinking correct?

Welcome to Biology.SE! Thank you for taking the [tour], but please also go through the [help] pages starting with [Ask] questions effectively on this site and delete or [edit] your question accordingly. In particular, questions must be focused enough to be answerable on this site — we cannot recreate textbook chapters! We also expect you to do research and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Your questions are both too general and based on imagination rather than looking up readily available facts. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Too many notes! Too many notes!

Transformation is done using plasmids right? So why are you concerned about recombination with the 'primary' bacterial genome?

@Roni Saiba im talking about the transformation as observed by Frederick Griffith's experiment in 1928 using virulent and non virulent strains of Streptococcus pneumoniae. Am I mistaken and does this type of transformation happen only through Plasmids?

@David im new to this website, can you please explain what are the " notes " you are referring to? ( I'm sorry if this somehow sounded rude, English isn't my first language )

Anish. Sorry for being obtuse. Welcome to the site. It's a good idea for new users to read the Help on Asking Questions. You should make sure that you are asking a single question about a problem in biology and set it out so we are clear what it is. This is a question and answer site, it is not a place to ask for comments on your general thoughts or difficulties with a topic.

@AnishKumar it is also good to have a question title that exactly states your actual question. For example you could ask "how does a completely foreign DNA recombine with genomic DNA during transformation/HGT". Also, as others suggested do not ask multiple questions (and ask one precise question) but it is good to provide a good background as you tried to do.


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Why don't bees sting hornets for defense?
Why don't honeybees sting hornets for defense when their hive is attacked? It seems like a good weapon against bigger animals - why not against hornets?

Can you provide a reference showing that they don't sting hornets?

@MattDMo I watched youtube video of japanese bees using heat to kill hornet but not sting.

Smithsonian mag says that the bee stings can't penetrate through the predator hornet's armor, which is simply a case of the hornet's armor being tougher than the blunt barb of the bee sting. https://www.smithsonianmag.com/smart-news/invasion-murder-hornets-180974809/
Here's a good research:"

To examine their behaviors of penetrating into different materials, we performed penetration–extraction tests and slow motion analyses of their insertion process. In comparison, the barbed stings of honey bees are relatively difficult to be withdrawn from fibrous tissues (e.g. skin), while the removal of paper wasp stings is easier due to their different structures and insertion skills. The similarities and differences of the two kinds of stings are summarized on the basis of the experiments and observations.

Some research suggests that bee stings have evolved to ward off vertebrates, physically and chemically. Wasps have more slender stings and perhaps that's why the hornets prefer bees nests.
Actually, a lot of insects have phenomenally hard keratin, beetles and the bulldog raspy cricket, as far as i know, even parasitoid wasps which have specialized stings evolved to cope specificially with insects are more common on caterpillars and spiders than strongly armored animals like big beetles.

Keratin or chitin? Insects have chitin exoskeletons.


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cell proliferation assays for research proposal
I'm an undergrad Biology student and I'm working on a research proposal for a certain course. I need help or guide on cell proliferation assays. I have a target gene , recent papers show that this gene's haploinsufficiency increases cell proliferation. However the most recent paper (published in 2020) showed that haploinsufficency decreases cell proliferation instead. I want to investigate this discrepancy but I don't know what methods should I use. In both papers they used immunostaining with Ki67 antibodies and SOX2 and TRB2 markers and in 2020 they also tested cyclin D levels. I'm not an expert at this field and I want to know what methods I can use for my experiment.
Thank You

There's no discrepancy between those results. Haploinsufficiency means only the gene on one chromosome is producing functional protein, not both chromosomes. Due to this lack of the protein, the cells increase their proliferation. However, in normal cells with both copies of the gene producing functional protein, cell proliferation decreases. That means this protein is a negative regulator of proliferation - if there's not enough of it, proliferation increases; if there's enough of the protein around, proliferation decreases. No discrepancy at all.

Sorry I didnt write my question right.. I meant that in one paper haploinsufficiency causes increased proliferation and in the other haplo causes decreased prliferation. In the last paper published they said that there is a discrepnacy and it needs to be further investigated

OK, that makes more sense. Can you please [edit] your question to clarify that?

It will also help if you can link the specific papers so that one can suggest a good experiment.


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Is there an example of a new species through mutation breeding?
Is there a demonstrable species that went through mutation breeding and through successive generations it drifted so far away from its initial parent species that it can't breed with them anymore? (I assume it would need to be able to breed with intermediate generations though). Also by "demonstrable" I mean a case where we can directly demonstrate this process by starting from a parent species to a new species and not establish this relationship by looking back (like observing the connection between corn and teosinte through genetic information).
Edit: I'm mainly curious about postmating/post- zygotic reproductive isolation. As I understand, the timescale of us is not enough to observe that kind of speciation (we can either directly observe the start of the isolation or the end of it but not both), that's why I'm curious about whether induced mutation could speed up the process enough to directly demonstrate speciation by the most difficult to achieve definition.
I have checked the thread Have we ever observed two drosophila lineages that evolved reproductive isolation in labs? but it seems to me that those results only shows premating isolation.
I have checked: Sexual and postmating reproductive isolation between allopatric Drosophila montana populations suggest speciation potential article which says, that postmating barriers observed may be due to postcopulatory-prezygotic mechanisms.
Thank you for the corrections, Im reading into Examples of creating a new animal species by humans

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). At a minimum, you should search on this site for related questions before posting to avoid duplicate questions. Please also see this sites criteria for "homework". Thanks!

There are also many other related questions on this site this one includes links to extensive documentation of such events.

Definition of species by the criteria of not being able to breed is problematic: e.g., some breeds of dogs cannot breed, due to the differences in their sizes, yet they are the sale species, as could be dhown by artificial fertilization.
Now, if we take any two closely related species and trace their genealogy deep in the past, we run into the same ambiguity: it turns out that at some point they could breed, and their separation into two dustinct species unable to breed was a process that lasted hundreds of thousands ir millions of years.
This brings us to another point: the characteristic evolutionary times for most animals are too long, compared to the existence of our civilization, for dustinc species to appear
This may not be true for faster evolving organisms, such as viruses or bacteria - e.g., HIV had diverged from SIV about hundred years ago. However we cannot define them as different species, except by saying that the dissimilarity if their genetic sequences exceeds certain threshold.


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Light intensity effect on plant transpiration
In the graph of light intensity versus rate of transpiration, the rate increases up to a certain point but then remains constant. What is the reason that it stays constant, is there a limiting factor such as water?

Can you add the graph you refer to to your post and add more backgrounds and a link to the source of your information?

The number of stomata on the leaf is the limiting factor. Light causes the stomata to open, more so with increasing light intensity. Once all the stomata are fully open, the transpiration rate rate cannot increase any further (for a given set of temperature and relative humidity conditions).


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How can I simulate heart electrical activity in a 2D plane?
I am not a biologist/medical student, I study software engineering. But I really like when medicine and engineering hold their hands together to achieve great things.
As a side/toy project, I was looking at creating a basic app that allows the simulation of the electrical conductivity of the heart (eg in the Left Atria), and to simulate some rotor drivers and fibrosis.

I got inspired by this Android App.
This app almost does what I want. Ideally I would like to extend this app to allow a more accurate model, allow fibrosis, allow pacing (i.e. manual intervalled stimulation of one point on tissue and see if it reveals rotors), and of course, allow manual ablation.
Unfortunately, this app has 2 issues for me:

I didn't find the source code of it, and I would not want to reverse engineer it and use it, even if just for fun, without any kind of consent. As a matter of principle, and I believe that all these kind of research should be open to the public by default, that's how Humanity evolves.

I don't know if this app is "too simplistic" in this simulation, I would like to use a more accurate model if possible (and still have this real-time simulation). I have seen tools such as OpenCARP, but they seem too heavy for a lightweight app, and I could not find a single tutorial showing how to make a 2D simulation of this kind of electrical activity, much less to do it in real-time and with user interaction. You can see that this app's rotors are not very accurate, as they do not depend on the tissue they conduct on, you can see as the simulation progresses, rotors are always generated at different spots, while in the real world rotors have a fixed location that corresponds to their core (which does not move constantly!), as depicted bellow:

So, it all boils down to: I will create my own app, inspired by that one, I will make its code publicly available, extend a few features and try to design it in a modular way such that other people can then easily extend it.
My ultimate question here regards the electrical physiology part of these simulators. And I need your suggestion: What is a good model for the electrical propagation, that I can use, that accounts for "fibrotic" obstacles, multiple rotors, etc.?
From a paper I have read regarding this topic, I found out they were using this model and obtaining some satisfactory results. Paper from that model.
I am still reading their paper, but their model seems complex to implement and probably will not result in any kind of real-time simulation (it seems it can take hours to simulate a single second of electrical activity).
So I would like to ask you what is the best model I could use for my app, that allows for a more real-time (not necessarily real, but at least allowing some 10fps, similar to the app), dynamic features (like different conductivity in different cells, fibrosis, manual pacing, rotors, etc.), being more accurate than what this app looks like?
Thank you!


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Do electric eels produce current as they just move about, and how/why?
https://www.youtube.com/watch?v=y9wktSQdyaE
This video demonstrates how an electric eel can supposedly produce up to 800 watts, and power a Christmas tree, which is very topical (a late Merry Christmas to the Biology community!). The video, sadly, is not very detailed as to how this works.
I was under the impression that electrical discharge was a conscious action on the part of the eel, rather than a natural state for it. But, apparently, the electric eel generates electricity "whenever it moves," as the video's narrator put it? Do electric eels produce electricity subconsciously, just by moving? Surely, though the host lists off the 800 watts of power, it's not constantly producing 800 watts, either?
How do the fish's electrocytes work in this instance, where just lazing about is powering the Christmas tree?

You are right - the 800 Watts are not constantly produced:
There are three types of electrical discharge: (i) low voltage (ii) high voltage doublets or triplets and (iii) high voltage high frequency.
(i) low voltage allows the animal to orient itself in its environment [b].
(ii) high voltage doublets or triplets are used for hunting: By discharging a high voltage doublet or triplet the electric eel induces involuntary twitching in the prey animal. Since this twitching is producing a weak electric field, this allows the electric eel to locate its prey. See Figure 3 of [b].
(iii) high voltage high frequency is used to incapacitate the prey. It's about 400Hz at up to 600V [b]. Wikipedia [c] states that these electric eel can produce about 1Amp of current. That's in the region of 800Watts the narrator is speaking of. Edit2: The pulse duration is about 1ms [e]. With a frequency of 400-500Hz this leads to a surprisingly high ~50% dutycycle. The ability to keep the frequency stable depends on the age (=length) of your eel: The older the eel, the more stable the inter-pulse interval.

Caption: Fig3 from https://doi.org/10.3389/fnint.2019.00023, red=50cm, green=75cm, blue=115cm length of eel
In Figure 5 of [a] you can see that the electrical eel is able capture prey in ~5 sec. During these 5 seconds the electric eel is pretty much constantly producing high voltage discharges. These could be used to light a Christmas tree.
To summarize: Yes - electric eels are very much in control of when and how they discharge. This can be quite clearly seen (or rather heard) in [d] which is  Supplementary Movie 8 from [a]
[a] https://www.nature.com/articles/ncomms9638
[b] https://s3.amazonaws.com/vu-wp0/wp-content/uploads/sites/182/2015/11/Science.pdf
[c] https://en.wikipedia.org/wiki/Electric_eel
[d] https://static-content.springer.com/esm/art%3A10.1038%2Fncomms9638/MediaObjects/41467_2015_BFncomms9638_MOESM559_ESM.mov
[e] https://www.frontiersin.org/articles/10.3389/fnint.2019.00023/full

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I wish I could bookmark this answer and upvote it again. Great work, dtadres!

@Johnny you can bookmark your own question just below the up/downvote buttons.