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Would the human body somehow get rid of very fine glass particle(s) that have penetrated the skin?
Assuming that a speck of glass dust has adhered to your finger and after a few days, you notice occasional discomfort when gliding your finger over surfaces (but non if you let the finger alone). It has improved somewhat but still persists lightly after approximately 10 days. If we assume that a single particle has penetrated the skin on your finger, possibly beneath the epidermis layer (meaning it can't be shed through the normal skin shedding process), are there any other ways the body can naturally remove it? Glass is inert, inorganic, and lacks direct receptors that the immune system can recognize. If it becomes encapsulated somehow, can that encapsulation eventually grow out (even under the epidermis layer)? Could it enter a blood vessel and migrate if it's very small?
Also many people say, it would be very unlikely that such things go in the blood stream and moves to the heart, but why is that the case? I mean as long as the particle is small enough, what blocks it to move with the blood stream? And if it really moves in the vessels, is there a natural way how the body could naturally eject it with time?
[This study][1] even notes, that glas particles

less than 20 μm disappeared within 1 year by becoming dissolved in animal clinical studies..

but how can the compounds constituting blood in vessels dissolve SiO2?? From laboratory work, what I know is that glas is very resistant, SiO2 is dissolvable with Hydrofluoric acid!!
[1]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4703599/#:~:text=Injected%20glass%20particles%20can%20travel,%3B%20Preston%20and%20Hegadoren%202004).

If we assume that a single particle has penetrated the skin on your finger, possibly beneath the epidermis layer (meaning it can't be shed through the normal skin shedding process), are there any other ways the body can naturally remove it? Glass is inert...

The vast majority of glass is inert, yes, but it's not sterile, and, as such, will lead to an inflammatory reaction encapsulating and eventually (if it's not deeply sub-dermal) expelling it with the outward growing epidermis and shedding keratinocytes.

Could it enter a blood vessel and migrate if it's very small?

Not likely. A shard of glass is very good at cutting/penetrating, but not very good at traveling due to its shape; it gets snagged on things. A very small shard of glass might lacerate or puncture a capillary or venule, but its shape and size would prevent most tiny shards of glass from entering the bloodstream and traveling remotely. Keep in mind that the internal diameter of an epidermal capillary is only 4–6 μm, and that of a collecting venule is 10–15 μm. While it's possible to have a shard of glass of 10μm, it would likely just injure the vessel, causing an inflammatory reaction that would wall it off and probably obstruct/close off the vessel. The only way I could think of to have glass shards in circulation would be to inject them directly into a vein, which has a comparatively large lumen.

if it really moves in the vessels, is there a natural way how the body could naturally eject it with time?

Assuming it is injected directly into a vein, it will get stuck somewhere in the circulatory system and will, through injury, cause an inflammatory response. It will get walled off, and walled off objects not directly under the skin or some surface (alveoli, gut) will just stay put, or the inflammation might cause a problem that the body deals with in another fashion.

...but how can the compounds constituting blood in vessels dissolve SiO2??

It doesn't get dissolved in blood; blood is relatively neutral. It gets dissolved over a long time in the inflammatory-induced encapsulation. How, exactly, I can't say, but I highly doubt that the pH in an environment where free radicals are produced is neutral.
I want to add that the danger from glass shards injected IV is mostly hypothetical, and has not to my knowledge been studied in vivo except once in 1947. The abstract in that paper states

This report on the effects of glass particles when injected into animals indicates that massive doses are required to produce damage to the organs examined during the study.

This is no reason not to use caution when aspirating fluids from glass ampules. Though I have never seen a problem from injecting such fluids locally (I wouldn't expect to be able to see what happens when injected into an IV as it would be remote), why not err on the side of caution? (Fyi: Rubber particles from needle insertion into rubber-stopped ampules results in loads more rubber microparticles in the fluid than glass in a single-use ampule.)
The role of macrophages in the resolution of inflammation
An In Vitro and In Vivo Study of Glass Particles in Ampules

Thanks, our body is awesome ^^ (that still sound a little bad "..walled off objects not directly under the skin or some surface (alveoli, gut) will just stay put". Just the idea that, for example, something from your childhood got trapped in your body and still is inside you and it's like a ticking bomb, maybe suddenly it causes damage somewhere out of nowhere  - scary)

@iwab - I'd say they (the walled off objects) are more like grenades with their pins pulled. The vast majority "rust" (get degraded) and are no longer able to hurt us. One of a few exceptions: tuberculosis, which can be reactivated.


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Does a tree absorb carbon dioxide only by its outer growth ring?
I'm trying to understand how the amount of carbon-14 isotope is changing in a tree trunk, so I would like to clarify if a tree absorbs carbon dioxide only by its outer growth ring in a current year of its life.

Welcome to SE Biology. Please finish reading the [Tour] to learn about this site. As an apparent non-native English speaker, I advise you to do what I do when writing in a foreign language. Run your text — especially the title — through a spelling and grammar checker before posting. Even if you are highly intelligent and your science is good, simple errors of grammar give a bad impression.

I think you will find that the CO2 is absorbed at the leaf, converted into sugars and then may be stored as carbon. So no Co2 at the trunk.

Do you actually mean to ask about CO2, or about carbon-14?

Thanks to everyone and sorry for my English, I'll try to be more careful with grammar next time.

@BryanKrause, I'm interested in carbon-14. I just know that CO2 contains carbon-14 at a constant percentage.

the outer ring stores carbon from the last growt season but the leaves store a lot too.

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Troubleshooting direct sandwich ELISA
I am validating an ELISA measuring A1c (also called glycated hemoglobin; target for humans) for use in another species. It is a direct sandwich assay. The standard and my sample (whole blood) were both serially diluted twofold.
I am wondering if anybody can help diagnose what I am seeing in my parallelism graph. As you can see, the curves are near inverse of each other (linearity R2 = -0.91). Since it is a direct assay, I would of course expect this correlation to be positive.

I have gone over my plate map and how I set up my dilution rack a hundred times in my head, and I am quite certain that I did load my plate in the correct sequence as my plate map - ie, having both standard and sample increase in concentration down their respective column. Is there any other possibility (besides me incorrectly loading my plate according to my map) that could cause this "perfectly incorrect" parallelism correlation?
I would love to be proved wrong and find out that it was indeed my error in loading - but I'm pretty sure I loaded it correctly...so I just wanted to check if there was any biological answer to this (matrix effect?)
I plan to run another plate tomorrow to check- but just wanted to ask.
Thank you!

It might be that there is a molecule present in your whole blood samples that masks your target epitope. Diluting the sample would also dilute the masking. But this is only one possible explanation, I guess there are more variables to consider to find a complete solution.

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Left digested peptides in speedvac for hours
I had done phosphopeptide enrichment of proteomic samples and digested the peptides with trypsin. However, I forgot and left the samples in speedvac to dry at 45 deg for way too long, about 10hrs. It does usually take a few hours to dry. Will it hamper my samples and the proceeding LC-MS analysis?
Another thing to ponder is that only one sample has a big round white powdery clump and the rest are transparent clear blobs, hard to see anything, as it should be. And this is also the tube which I eluted one extra time as well. If it is salt or detergent I don't think it would be that thick. Have any idea on what this could be? I will run it in the MS anyway. Thanks!

Sounds like it's unlikely to work, to me, though I'm not an expert in this stuff. Interested to hear what the data look like though!

Thank you for responding and for your insight. I will run it in the MS soon and see. I hope it somehow works and will update on how it looks, fingers crossed.


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What is the mechanism by which an animal has behavioral instincts?
I understand (at a layman's level) how evolution and natural selection work in regards to anatomy.  The offspring has a slight mutation that makes it a better survivor in some way -- faster, stronger, more agile, better camouflage, more efficient respiration, whatever.
But I have no idea how instinctual behavior is developed and/or transferred.
Observing my house cats, I can see that they have all kids of instincts for hunting, fighting, playing, grooming, etc etc.
Where did these instincts come from?  Animals (including humans) are born already knowing a lot of things, right?  That's what "instinct" means.
How does that work?  Do we even know?

Instincts are formed the same way anatomical attributes do: genetically. The nervous system has developed instincts (or reflexes, if it helps you to understand them better) through millions of years of selection; those individuals with beneficial instincts had a better chance of survival to reproductive age.

@anongoodnurse So instincts are also anatomical differences, localized in the nervous system?  And organisms with "bad instincts" died out?

I believe so, yes. Instincts can mean different things to different people, so there's room for debate. They can be said to be genetically coded for neurologically, though they can also be altered by the environment. A neuroscientist might argue that there is no one satisfactory explanation for instincts, but that we are born with many of them is irrefutable. Dogs bred over time to hunt and kill small animals (e.g. vermin) will have a very high prey drive whereas those bred solely for companionship may have a very low prey drive.

This site has a policy of the OP showing evidence of research (e.g. links to an article and a quote) in an attempt to answer the question; if you [edit] your post to include some, you may get a much better answer than mine. I think it's a very interesting question.


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Is this a wandering spider?
I recently visited the Peruvian Amazon near Puerto Maldono and found this spider. Can someone please help me in identifying it? It was about 7cm in length, including legs.
I hope that it might be a wandering spider, but idk maybe it could be a massive wolf spider or some other spider…?
I poked its leg gently with a long piece of grass and it didn’t flee, but raised it’s front two legs (only slighly though) as I’ve seen wandering spiders do in videos, and I’ve never seen wolf spiders do this?
Idk if this helps, but anyways, would love some help!

Nice! It's not a wolf spider; the eyes are wrong for that. I think it is; the single dark line on the dorsal carapace and the striped palps certainly suggest Phoneutria, but I'm not sure, so this is a comment, not an answer. It may not have felt threatened enough to go full-on upright. I hope someone else knows.

Yes.

Ctenidae, number 7 on this graphic, have a distinct eye pattern from the wolf spiders (lycosidae; number 1).
I couldn't tell you the species, though.

Awesome, thanks so much for the help!

Just in case you're curious, the largest wolf spider that you'd likely find in Peru is probably Lycosa erythrognatha, which doesn't get much more than 4-5ish centimeters across.


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Why does the nucleus not exist in mature red blood cells?
I'm currently a high schooler learning biology. I just wanted to know why does the nucleus not exist in mature red blood cells. It would be great if someone answered my question in a basic way as I have not learnt it in depth yet, just wanted to understand the basics first. Thanks in advance for your help. :)

Hi Iris, and welcome. Is there no explanation in your book? Did you do an internet search in an attempt to answer this? Evidence of research (e.g. a quote and a link) is required on this site. Do you want to know how enucleation occurs, or why? The "why" is that that's what evolved in mammals because it conferred some kind of advantage at some point (the "why" will be a teleological reason). Please read about it and ask a question about something specific that you don't understand with a quote from and a link to the source. Thanks.

This paper might help, especially the second paragraph of the introduction section.

worth noting this is only true of mammal red blood cells. avian red blood cells for instance have nuclei.

Well, a cell requires nucleus for growth, modification and maturation. Once the cell has attained its size and functionality, nucleus is not a necessity. As you know RBCs carry oxygen (also carbon dioxide in a different form, about 20 -25 percent), space is required for it. So, to increase the capacity of the RBCs to carry more oxygen, by increasing the space to accommodate more haemoglobin, nucleus is destroyed in an RBC. The avg. lifespan of an RBC is 120 days. so, for 120 days, it can function without the nucleus. You may think of other examples of cells that don't contain nucleus like Sieve cells of phloem etc.

You might benefit from reading the second paragraph of the introduction linked to in the comment below the question as well. You're answering with hypothesis, not accepted fact (though it is often presented as fact.) Why are mammals the exception to nucleated blood cells? Are avian RBCs less efficient than mammalian RBCs?

Hmm, evolution of birds and mammals is not along the same line. Also, camels and llamas have nucleus in their RBCs. The answer I provided may not be the fact, but the person requested a simplified answer do I tried to provide the answer simply. By the way, thanks for the paper. I shall definitely go through it.

You've missed the point entirely. Mammalian RBCs are no more efficient than avian RBCs, so your answer doesn't make any sense. Also, camel RBCs are enucleated. Don't trust the superficial sources of info on the internet

Would you please elaborate.

I don't believe in giving an entire ocean when one asks for a glass of water. For initial reference one should go through the most well accepted hypothesis even if it may be not completely true. You pointed that camel don't have nucleus but what about llamas? Same/similar selection pressures might have several possible outcomes and routes.

Clearly you're unaware that llamas also have RBC's without nuclei. Before you ask, so do alpacas, vicuñas, and guanacos. You've been wrong three times now. What has your observation about birds' evolution got to do with my comment about red blood cells? Your answer isn't an ocean, but it also isn't correct.

Ya, i acknowledge that my answer is wrong. I came to know that the dark structure of their RBCs in not nucleus but some sort of microtubules or something. But the conventional yet wrong answer is the answer given by me. Thank you.


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How is opsin of rhodopsin is different from that of iodopsin?
Rhodopsin contain retinal, an aldehyde of vitamin A and opsin protein and iodopsin also contains retinal along three different types of opsins namely erythropsin, chloropsin and cyanopsin. But kind of opsin does rhodopsin has ?

You'll need to clarify what you mean to ask.

What I want to ask is, like in iodopsin, there are three different types of opsin protein erythropsin, chloropsin and cyanopsin. But in rhodopsin we have retinal and opsin but how is this opsin different from the opsins of iodopsin ?

Different how? What sort of differences are you looking for?

See, rhodopsin consists of retinal and opsin which on separation of which we are able to perceive light. Now in case of iodopsin which is found is cones also contains retinal and three different kinds of opsins namely chloropsin, erythropsin and cyanopsin. Now the opsin that we find in rhodopsin, how is it different from these chloropsin, erythropsin and cyanopsin that are found in iodopsin ?

How is it different how? Imagine you have cats and dogs and you want to know how they are different. The list would be endless: you could talk about how they make different sounds, have different diets, their color, the texture of their fur, their history of domestication, etc. Which characteristic of these opsins are you asking for a comparison of?

I'm asking how they're chemically different ?

They're different proteins; they have different amino acids. Is that what you want to know?

Yes, what kind of groups they have in their structure ?

What do you mean by "groups"? What are you trying to learn or do?

I'm talking about functional groups such -CHO, -OH, -CO- etc that we usually find in organic compounds.

There are a few hundred amino acids in an opsin protein; each are going to have one or more of those functional groups in addition to the amino backbone.


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What makes viruses like the flu and covid so tolerant of mutations compared to most other viruses?
I was curious about why we benefit from yearly flu shots and apparently will also benefit from yearly covid booster shots too, whereas this doesn't seem to be the case for most other vaccines -- even if a booster or multiple booster shots are needed, it's typically a set sequence of shots, such as 3, with a month between each one.
I already know the surface level explanation is that these two virus' evolve and mutate very quickly.  However that doesn't explain WHY they mutate so quickly or why such much constant mutation doesn't frequently end up being fatal to the virus or destroying its ability to reproduce, or even just do nothing helpful or harmful.
I did find this article: Why We Get Annual Flu Shots—and How Universal Vaccines Could Knock Out Viruses, which states that

flu and coronaviruses seem to be very tolerant of change. For a virus to change and still be capable of infecting a host population, the virus must maintain critical functions such as attaching to host cells. A high rate of change must be combined with great tolerance for transformation. Most viruses aren’t like that at all.
“With many viruses, when mutations crop up, they just kill the virus, and that’s the end of the show,” Hensley said. Not so with flu and coronaviruses. “Flu and SARS-CoV-2 have this uncanny ability to acquire mutations and still be able to replicate efficiently,” he said. “These viruses evolve to avoid human immunity while maintaining functions critical for viral replication.”

I don't understand why though.  What makes these particular species both so fast involving and so resilient in the face of mutations?
Edit: Also, just to be clear, I understand the probabilistic nature of an organism getting a useful mutation -- that, even if most mutations would either hinder an organism's ability to reproduce (either by directly killing it off, or just making it harder to reproduce) or have no effect, given a sufficiently large number of the relevant organisms repeatedly reproduce for a sufficiently long time, it's unsurprising that a few members of the species emerge that, by chance, happen to have some mutation that increases their ability to reproduce, and they pass on the mutation to their offspring (not sure if that's the correct term when talking about asexual reproduction, especially with viruses since they can't even reproduce at all without hijacking the cellular machinery of some other organism), and so on.  That's just natural selection, if I'm remembering my terminology correctly, and I understand the basic idea behind it, so I just wanted to clarify that that isn't what I'm asking about.  Instead, I'm asking what specifically distinguishes flu viruses and the various variants of covid from other viruses (and even from just other RNA virus) that specifically makes them more resilient to mutation.

"why such much constant mutation doesn't frequently end up being fatal to the virus or destroying its ability to reproduce" It does, actually, it does so much that the vast majority of viral particles produced, are effectively worthless.

What is it that you want to know? Why RNA viruses undergo more mutations than DNA viruses or what one individual means by “toleration of mutations”? We can answer the former, but the latter is scientifically meaningless.

This is actually a far more complex question than it might seem on the surface. It's something that has been noted for quite some time by virologists - and it isn't just RNA viruses that do this. Almost all viruses (at least for the mammalian viruses that I know of) seem to produce mutants at some rate and many of the virions produced are non-functional for some reason.
RNA viruses mutate at high rates because it is an inherent property of the mechanism that replicates these viruses, actually it's an inherent property of all RNA replicating machinery. In most RNA viruses the mechanism is a multi-component protein known as a RNA-dependent RNA polymerase, and is inherently error-prone. You can see the details of how they work and the structures in these excellent reviews by Fodor and te Velthuis1 for influenza and Hillen2 for SARS-CoV-2. SARS-CoV-2 has some form of error checking/proofreading3 in the system, but this isn't perfect, as it isn't for DNA polymerases either, so this answer applies to most viruses.
However, what is important here is not the mutation rate as such, but the fact that these viruses are incredibly infectious. You only need a few viral particles to infect - for some influenza viruses this might be as low as about 40 particles4, but more typically a bit higher than that. During an infection, viruses such as influenza and SARS-CoV-2 are putting out about a billion (109) and 100 billion (1011) particles5 - that's an enormous number, even if you take an infectious unit to be 1000 particles, then you still have about a million or so of them. This also means that even if a huge chunk of that number is defective in a manner that inhibits replication, then it doesn't matter; you are still going to get infection and replication of those that are capable of it.
Viruses of this sort exist as what is known as a quasi-species - basically think of it as a cloud of viruses with similar genomes. Some of those genomes are defective at replication because they are missing significant or crucial chunks of the genome (packaging faults or problems resulting from recombination for example) or packaged with defective proteins, some are defective because they have a mutation in a critical site, and some are defective because of mutations that alter protein structure or cause premature termination of protein products.  There is of course, extremely strong selection pressure for genomes with no mutations or non-critical mutations in those critical locations. How this is achieved is through the use of redundancy in the genetic code; silent mutations have no effect for example, or it might be that substitution with a similar amino-acid has little to no effect. In some viruses it is thought that the ratio of replication competent virions to defective is in the order of 1:100 (i.e. 1 replication competent:100 defective), and sometimes even higher. You can actually generate higher ratios by serial passage of undiluted virus stocks, because the defective particles are often generated faster than replication competent particles due to shorter genomes
So, you might be asking - but what about all those defective particles, what are they doing and why would they be produced? Well, some of them are indeed infectious, but not capable of producing fully replication competent virus themselves, so produce a dead-end infection. These are sometimes called things like Defective Interfering Particles. There's some debate about what they do exactly, but it seems that they are drivers of the virus-host interaction in some manner6. They have been found in almost all viruses and they seem to be produced consistently and not produced under certain conditions, which probably indicates that they are important for infection in some way, whether it be mopping up the immune response to allow a better chance for replication competent virus, or some other mechanism.
References:

Te Velthuis AJ, Fodor E. Influenza virus RNA polymerase: insights into the mechanisms of viral RNA synthesis. Nat Rev Microbiol. 2016 Aug;14(8):479-93. doi: https://doi.org/10.1038/nrmicro.2016.87. Epub 2016 Jul 11. PMID: 27396566; PMCID: PMC4966622.

Hillen HS. Structure and function of SARS-CoV-2 polymerase. Curr Opin Virol. 2021 Jun;48:82-90. doi: https://doi.org/10.1016/j.coviro.2021.03.010. Epub 2021 Apr 6. PMID: 33945951; PMCID: PMC8023233.

Moeller NH, Shi K, Demir Ö, Belica C, Banerjee S, Yin L, Durfee C, Amaro RE, Aihara H. Structure and dynamics of SARS-CoV-2 proofreading exoribonuclease ExoN. Proc Natl Acad Sci U S A. 2022 Mar 1;119(9):e2106379119. doi: 10.1073/pnas.2106379119. PMID: 35165203; PMCID: PMC8892293.

HORSFALL FL Jr. Reproduction of influenza viruses; quantitative investigations with particle enumeration procedures on the dynamics of influenza A and B virus reproduction. J Exp Med. 1955 Oct 1;102(4):441-73. doi: 10.1084/jem.102.4.441. PMID: 13263486; PMCID: PMC2136520.

Sender R, Bar-On YM, Gleizer S, Bernshtein B, Flamholz A, Phillips R, Milo R. The total number and mass of SARS-CoV-2 virions. Proc Natl Acad Sci U S A. 2021 Jun 22;118(25):e2024815118. doi: 10.1073/pnas.2024815118. PMID: 34083352; PMCID: PMC8237675.

Vignuzzi M, López CB. Defective viral genomes are key drivers of the virus-host interaction. Nat Microbiol. 2019 Jul;4(7):1075-1087. doi: 10.1038/s41564-019-0465-y. Epub 2019 Jun 3. PMID: 31160826; PMCID: PMC7097797.

It would be interesting to see the solution to the detailed combinatorial problem of transmitting a collection of P infectious particles from a relatively homogeneous (?) pool in the source organism. The number of particles in the source is so huge that it doesn't really matter. What matters is the likelihood of those P particles being emitted and then arriving together at the target.

@BuckThorn I think you might have a bit of a misunderstanding of the transmission problem - the viruses don't transmit as a single virion; the air is too dry for many viruses to survive more than a few seconds, and they are coming from a very wet environment. They transmit in in areosols - tiny (and not so tiny) droplets etc from sneezes, talking and even breathing. Each aerosol will contain some virions, I would guess the number correlates somewhat to aerosol size.

No, I understand that this is the transmission mechanism. But does it matter if the virions travel together in one aerosol particle, or can they be in multiple? And how closely related (genetically etc) are virions in one particle. Is the original pool in the source uniformly mixed? There are many such interrelated questions. Ultimately the likelihood of virulent transmission becomes the product of the likelihood of the individual events, but you obviously have to know what the individual events might or must be.

@BuckThorn I suspect that I'm not enough of a mathematician to understand fully. There are a bunch of virologists working on modeling of transmission in most common species, but I don't remember the specifics from my time in influenza.

Don't mean to keep the comments flowing too long, but what triggered my comment was reading about the mindboggling number of virions that a host might harbor, and the possibility that many if not most of those virions might be defective, as you describe.

@BuckThorn in that case the assumption would not be homogeneity - the aerosols will contain virions from the region where they originate. Assume a random population of non-infectious particles from each cell, and I think roughly the same population across cells (people have compared single cell infections in influenza). Some selective differences across the lung though - differences in attachment factors (sialic acids for influenza) in different parts of the lung. Strongly depends on the virus though. Might make a good new question here.

One consideration is that influenza viruses and coronaviruses are RNA viruses. While DNA viruses are generally dependent on the host's replicative enzymes, which have evolved low error rates for host fitness, RNA viruses encode their own enzymes for replication, allowing optimization for viral fitness [1]. High mutation rates allow for high population-level diversity and therefore adaptability, and RNA viruses have evolved high error rates on the order of 10-4 to 10-6 (compare with 10-6 to 10-8 for DNA viruses [2] and 10-8 for humans [3]).
This leads to your question of how RNA viruses tolerate such high mutation rates without entering an error catastrophe in which the accumulation of deleterious mutations becomes lethal. This tolerance of error is referred to as genetic robustness, and there are several mechanisms by which RNA viruses achieve this (the following is based largely on [4]):

Population size - Most importantly, RNA viruses replicate very quickly and very often, leading to extremely large population sizes [5]. Even though deleterious or lethal mutations occur frequently, there are still a large number of individuals with neutral or beneficial mutations that will survive [4].
Multiplicity of infection - A single cell can be infected by more than one virion, allowing a non-functional protein from an allele in one genome to be complemented by a functional protein from an allele in another [4].
Recombination - Related to multiplicity of infection, RNA viral genomes can recombine [6] and this could potentially allow deleterious mutations to be unlinked from neutral or beneficial ones [4].

Although points 2 and 3 would also apply to other types of viruses, multiplicity is also influenced by the large population size of RNA viruses. High viral copy numbers within a cell could give a greater potential for recombinational rescue of deleteriously mutated genomes, and, since mutated copies of a viral genome can also be translated [7], they can also therefore complement one another even in cellular infections initiated by only a single virion.

NB: Several of the Wikipedia links aren't really applicable to what is being discussed here, but I included them anyways because they're about vaguely similar concepts.
References
[1] Duffy S. 2018. Why are RNA virus mutation rates so damn high? PLoS Biol 16(8):e3000003
[2] Sanjuán R, Nebot MR, Chirico N, Mansky LM, Belshaw R. 2010. Viral mutation rates. J Virol 84(19):9733-9748
[3] Nachman MW, Crowell SL. 2000. Estimate of the mutation rate per nucleotide in humans. Genetics 156(1):297-304
[4] Lauring AS, Frydman J, Andino R. 2013. The role of mutational robustness in RNA virus evolution. Nat Rev Microbiol 11:327-336
[5] Moya A, Elena SF, Vracho A, Miralles R, Barrio E. 2000. The evolution of RNA viruses: A population genetics view. Proc Natl Acad Sci USA 97(13):6967–6973
[6] Wang H, Cui X, Cai X, An T. 2022. Recombination in Positive-Strand RNA Viruses. Front Microbiol 13:870759
[7] Boersma S, Rabouw HH, Bruurs LJM, Pavlovič T, van Vliet ALW, Beumer J, Clevers H, van Kuppeveld FJM, Tanenbaum ME. 2020. Translation and Replication Dynamics of Single RNA Viruses. Cell 183(7):1930–1945.e23


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Experiments on the effect of pruning a tree on water uptake and soil drying
Having a street tree close to my property and being concerned at the risk of subsidence, I am trying to understand whether and to what extent pruning of the tree might help to reduce the risk (I appreciate that other factors - tree species, soil type - are also important). From an online search I found a number of sources offering an opinion, but it was not so easy to find advice based on scientific experiment.
However, I came across the report Controlling water use of trees to alleviate subsidence risk (2004) describing a project led by a consortium including East Malling Research, the University of Cambridge, and others. This describes experiments in which two pruning techniques, crown-reduction and crown-thinning, were applied to trees over a period of years, and measurements were undertaken of the effects on transpiration and soil drying. The results broadly suggested that pruning was not a very effective method of reducing soil drying.
Crown-reduction, reducing the volume of a tree while preserving its shape, was found to reduce total water use of a tree in the year of pruning. Soil drying was also reduced in the year of pruning, but only to a small extent, and not at all in the following year unless the reduction was severe. It was also found that crown-reduction: a) led to re-growth with larger leaves arranged closer together; b) these leaves had a greater capacity to lose water.
Crown-thinning, removal of some lateral branches while preserving the overall size of the tree, was found not to reduce soil drying.
A limitation of the study was that the experiments on pruning were undertaken on just two species, wild cherry and London plane.
Question Have any subsequent experiments on the same or other tree species either confirmed or differed from these findings?

The obvious questions here are when was the tree planted and how big is it? The risks would be quite different for different trees I would have thought because of the different sizes, transpiration rates etc.

@bob1  About 12 years ago, and about 10 metres high.  But I mentioned the tree close to my property just as part of the background to my question about experiments on the effect of pruning trees.


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Can Palisade Cells Survive Independently?
I have been intrigued by this question. Can palisade cells survive independently from its parent plant in a chemical environment? For example, if we were to separate a palisade cell from a plant and place it in sucrose solution, how long would it survive?

Yes they can. In 1902 Haberlandt reported single palisade cell culture from leaves in knop’s salt solution. Now there are many different methods of plant tissue culture
for PLANT TISSUE CULTURE see

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Is the amount of phosphoric acid added to colas enough to disrupt the function of the kidney over the long term?
Both Coca-Cola and Pepsi add phosphoric acid $H_3PO_4$ to their colas to give them a signature "bite".
The kidneys use a phosphoric acid/dihydrogen phosphate/hydrogen phosphate homeostasis as one mechanism to eliminate/excrete excess acid from the body.
The issue of whether sodas containing phosphoric acid can exacerbate osteoporosis and related conditions has been explored here and in some detail on Wikipedia, but I'm more interested in direct effects on the kidney.
I'm interested to know if the overall renal physiology is adversely affected by extra phosphoric acid that long-term moderate consumption (say a single 2L bottle per week for a year) of soda would introduce (including interrupting or saturating the Na-Pi transporter)?

Could you define "long-term"? Say, one 200ml can of soda/day for 10 years?

@nico That's a good idea.  I was trying to make it more abstract and less "medical advice"y.

It's just that I have the feeling that the result would vary a lot depending on the frequency of assumption (not that I have any data whatsoever regarding this issue. Very interesting nevertheless!)

The phosphoric acid in cola will contribute to dietary intake of phosphate. I may be missing something, but, since the transporter functions to reabsorb phosphate that has been filtered out at the glomerulus, excess phosphate will spill over into the urine.
According to Wikipedia the RDA for phosphorus is 700 mg and the tolerable upper intake level is 4000 mg. Coca cola contains 17 mg phosphorus (as phosphate) 100 ml-1 (which is 340 mg in 2 L)
According to this source,

in the United States, an average person drinks 412 8-ounce drinks — or 3296 ounces — of Coke per year.

This works out at 9 oz per day = 266 ml = 45 mg phosphorus
For comparison (from here):

white flour contains 595 mg 100 g-1
one boiled egg contains 220 mg
canned salmon contains 240 mg 100 g-1

No, you didn't miss anything, great answer!  I was thinking about the precision of the acid-base balance of that particular system being disturbed (realizing, of course, that it potentially only handles "spillovers" from the bicarb system, I think).  It's interesting to see the comparison of the content with other foods, though I'd be curious about how much of that in the egg, etc., is AMP/ATP and others.

Brain fart on selecting this as the answer, sorry for the delay.

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What is a inhibitory tone when talking about neurons?
In this SE answer: Could an "overactive" brain increase the chances of Alzheimer's Disease?
user @nico used the word inhibitory tone What does that mean?
More examples of it used:
http://www.ncbi.nlm.nih.gov/pubmed/18234887
http://www.cell.com/neuron/abstract/S0896-6273(11)00479-X

Neurons communicate electrochemically. That is, when a signal arrives to a neuron it fires a series of electrical signals, called action potentials.
Action potentials are depolarization events that propagate along the neuronal membrane, down to the neuronal terminal.
The terminal of a neuron is (with some exceptions) in contact with another neuron, via a structure called synapse.
When the depolarization arrives at the terminal, it allows the entry of calcium, which then mediates the release of a chemical substance, a neurotransmitter into the synaptic space. Finally, neurotransmitters act on the postsynaptic neuron, by binding to specific receptors on its cell membrane and can either stimulate it, in which case the postsynaptic neuron will fire more and release more of its neurotransmitter or inhibit it, in which case the opposite happens.
The textbook example of a stimulatory neurotransmitter is glutamate, and the inhibitory one is GABA1.
In various areas of the brain certain neurons are constantly receiving inputs from GABAergic afferents. This means that those neurons are constantly receiving a GABA stimulus that inhibits them, and are thus under a constant inhibitory tone. This will prevent their firing until a sufficiently potent stimulatory stimulus arrives or until the inhibitory tone is somehow released (for instance if the inhibitory GABAergic afferents are themselves inhibited by some of their own afferents).

1note that this is not always true: GABA can also be stimulatory in various situations


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Is it possible to improve metabolic rate through quorum sensing?
I am building a microbial fuel cell unit using mint plant and soil microbes. My goal is to power a LED light using the electricity but the electrify that microbes are so little so I am thinking of methods to fix this with quorum sensing
Currently, I found that riboflavin could potentially enhance the production of biofilm through quorum sensing. Have anyone tried this approach out yet? Or are there other recommend methods that could help this process? Huge thanks in advance!!

Welcome. We ask questions to be accompanied by some background research, this helps to focus the question to something answerable. The current question is too open-ended and we are not a discussion forum. What have you found so far on this topic?


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Why doesn't the Goldman Equation take into account ions that have no permeability?
While I was studying the Hodgkin-Huxley model, I encountered an a phenomena that confused me a lot.
I couldn't find the answer myself, so I wanted to ask here.
While calculating the equilibrium potential with the Goldman equation, why do we neglect the ions to which the cell wall is impermeable?
Let's say there is only sodium solution on both sides and only sodium can pass through the membrane. After the equilibrium state, if we add potassium ions to the side where the potential is high (let's say inside in this example). Outward sodium current must occur because the force resulting from the electrical force and density difference is not in balance (due to the increasing strength of the electrical force).
In the last case, the sodium density difference (and therefore the external/internal ratio) changes, but according to the Goldman equation, the voltage should not change because the added potassium cannot pass through the membrane.

No one has a bucket of potassium ions to add to solution. Whenever you have potassium ions you have some anion along with it.

The equation is for biological systems and as Bryan has pointed out, charged ions cannot be unilaterally added on either side of the membrane and ions are always accompanied by an opposite charge.
Biological fluids are neutral. So why is there polarisation of membranes?
This is because of the sodium potassium pump that consumes approximately 30% of ATP at rest! It maintains a gradient of sodium and potassium on either side(sodium being higher on the outside and potassium on the inside). But again the fluids are neutral as i mentioned. Sodium on the outside is offset by anions and so is potassium intracellularly.
Read this carefully now,
the diffusable ions form a very thin layer of charge on either side of the membrane like a capacitor. As the layer is very thin, only a few ions are required to move on either side to change the potential making the process of depolarisation and repolarisation of membranes very rapid. Resting membrane being permeable to potassium only, potassium diffuses out along its concentration gradient(establised by the Na-K pump) and quickly settles on the outside of membrane creating a positive charge on the outside and the electrostatic gradient balances the concentration gradient. Therefore at resting state membrane potential is determined only by concentration of potassium on either side of membrane. That's why we are so concerned about hypokalemia and hyperkalemia states in our body.
When sodium channels are opened due to stimulus, sodium rushes along its concentration gradient until it is offset by electrostatic force in a similar manner. As soon as the channels close, potassium again restores the original state by diffusing out.
Hope this helps, i struggled with the same doubt earlier until a friend of mine explained it to me.


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Rifle Bullets and Lead Exposure
Does anyone know if simply touching bullets could give you lead poisoning?

Simply touching bullets couldn't give you lead poisoning, since nowadays bullets are usually coated in a protective copper shell.
What makes bullets dangerous isn't the actual bullet but the way lead is expelled from it upon shooting.

When a bullet is fired, it gets so hot that that lead actually vaporizes.
  ~Sarah Zhang
  http://www.motherjones.com/blue-marble/2013/01/lead-shooting-ranges-osha

Thus, just touching the outside of a bullet wouldn't be damaging. The only real ways to get lead poisoning would be by inhaling lead in the air - but even that would have to be in large amounts - or by touching lead directly and then putting your finger(s) in your mouth and ingesting it.
See this link for more information.


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How is instinctual information encoded?
If instincts are passed on through genetics, how is that information encoded in DNA?
For example, spiders instinctively know how to spin webs. Does that imply that the algorithm for web spinning is directly encoded in spider DNA?

related: http://www.physicsforums.com/showthread.php?t=280432

Web spinning in spiders is a complex behavior and probably involves a number of different factors, genetic and environmental. Genetically there are surely many different genomic regions underlying the development and expression of the behavior.
Is the algorithm for web spinning directly encoded in the DNA? Not directly. There is not a single region of contiguous DNA sequence that codes for all the steps involved in building a web. Instead, there is a sequential and parallel developmental process beginning at fertilization (earlier if you include parental epigenetic modifications) - encoded and regulated by the genome and its products - that, without too many errors, generates a viable and fertile web-spinning organism. But the DNA sequence involved in that algorithm is spread all over the genome and includes coding genes, non-coding (ncRNA) genes, and regulatory regions. And the genome alone will not carry out an effective algorithm without proper environmental inputs like nutrition and parental provisions.
The act of constructing a web, when and where, and the design of the web is likely carried out via brain architecture and neuronal patterning, but of course these structures are built based on the DNA-based, developmental algorithm. In that sense, there are many nested levels of algorithms.
One of the best models used for studying behavioral genetics is the fruit fly Drosophila. Many different behaviors have been studied at the genetic and molecular level in Drosophila including courtship, foraging, sleeping, and memory-related tasks. A popular science book on behavioral genetics worth checking out is Time, Love, and Memory by Jonathan Weiner. It details the work of Seymour Benzer and provides a lot of background and easily understood explanations of how genes and their products can work together to exhibit complex phenotypes like sleeping patterns. It includes a detailed (though not up-to-date) description of circadian gene circuitry and how it develops.
At the moment, the best that I can think of for an algorithm directly encoded for by DNA is the sequential activation of HOX genes for animal body plans. But even in this case DNA code does not progress through correct development without other factors.

+1 sound good, do you have any primary references?

Thanks, Abe. If you're looking for some hardcore data, the most interesting paper I've read recently, and that I enjoyed, investigated how innate courtship behavior is modified by learning. Besides characterizing the changes in behavior based on experience, it described the genetics and cell biology that regulates the behavior. http://www.nature.com/nature/journal/v489/n7414/full/nature11345.html

Regarding web-spinning: after a quick search through pubmed, there really isn't much literature on the behavior. The genetics and transgenics of silk production is heavily studied (you may have heard about silk-producing goats), but nothing detailed about web construction. There have been studies on web making by intoxicated spiders. You can find some primary sources from the wikipedia references. http://en.wikipedia.org/wiki/Effect_of_psychoactive_drugs_on_animals


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What part of the cactus photosynthesizes?
In general, plants photosynthesize through their leaves and, to a much lesser extent, through their stems. Cacti, however, have no visible leaves, but instead spines. In what part of the cactus does the photosynthesis take place?

Since photosynthesis is correlated with chlorophyll, I'm guessing the green part.

In wiki there is a good answer for your question http://en.wikipedia.org/wiki/Cactus#Leaves
In plants photosynthesis takes place in chloroplasts. Chloroplasts may be in the cells of fruits, stems, but most of all in leaves. In some succulents (such as cacti), the main photosynthetic activity is associated with a stem.


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Risks of latent viruses that reside in ancient genomes under research?
Some interesting research in reactivating mammoth genetic material (https://www.nature.com/articles/s41598-019-40546-1) made me wonder what risks are inherent (or are not inherent) in reviving older genomes that may have integrated latent viral code?
Are there potential biohazards in this line of research, where dormant viruses that have otherwise gone extinct (along with the extinct host) and which now may have the potential to be reactivated? Not just in terms of zoonoses that infect across species, but also viruses that infect modern animals that are more closely related or have relatively common ancestry (e.g., from mammoth to elephant).
Could a disease be brought back via this kind of research? Or are the conditions for waking latent viruses from starting material of this kind just not possible to recreate in a lab setting?
Edit: To clarify what I mean by potential biohazard in relation to this question: Experimental conditions result in a latent virus going into lytic phase. The virus is a communicable pathogen; it spreads outside the laboratory environment; it causes sickness or death to living organisms to the extent that it creates a public health, ecological, or other crisis of significance. For background, please also see: Cambridge, The Free Dictionary, and Wikipedia.

I'm sure the extent to which this might constitute and answer, but scientists have in fact resurrected (to some extent) viruses that were otherwise extinct, including an influenza virus and an endogenous retrovirus.

First, I don't understand why you are more worried about viruses of extinct species, instead of ancient viruses of species that haven't gone extinct. Clearly the infectious potential of the latter is greater for the current species. I haven't heard a peep in published literature about the dangers of resurrecting mammoth viruses, but surely recreating (in 2005) the 1918 influenza
did stir some fairly substantial safety debates.
In general, working with ancient DNA (aDNA) does require some safety precautions, but mainly because of the risk of contaminating the aDNA (with modern DNA)-.
Furthermore, I'm not aware of any research having resurrected an ancient virus from an extinct species aDNA (your specific scenario), but one ~5-million y.o. retrovirus (dubbed Phoenix) was assembled from current human DNA (in 2006); the authors were a little worried as to its infectious potential, so they engineered it so it couldn't replicate more than once.
More commonly, the genome of less ancient virus strains is being fairly routinely reassembled from e.g. from mummies, skeletons, or even packrat middens in order to study the evolution of common viral diseases. Most of this goes on without any safety controversies, as far as I can tell. Less commonly, ancient viruses of various species are found fairly intact in permafrost which does also stir some safety discussions (regarding the handling of permafrost).
So is your scenario possible in theory? Yes. Are experts worried about it? Not that I've heard...

About your leading sentence "...I don't understand why you are more worried..." There's no evidence of that being the case in the question whatsoever; it seems personal, gratuitous, and unnecessary. But nonetheless, +1 for the "...the authors were a little worried..." example.

If you would like to edit your answer to include just what is relevant to my question, I'll be happy to mark your answer as "accepted". Thanks again for answering!

@AlexReynolds: and what would that be? There's no research or even an opinion (except mine) directly on your question. It's circumstantial evidence (on related issues) basically supporting my opinion.

Are there potential biohazards in this line of research, where dormant
  viruses that have otherwise gone extinct (along with the extinct host)
  and which now may have the potential to be reactivated?

There are always potential biohazards. If you dig into the unknown, you can't tell in advance what you can find. Said that I would like to point the attention to the fact that we don't know all the viruses already in existence, nor the ones that evolve every day.
You get in contact with new viruses during your everyday life anyway. How much more hazard would come from ancient viruses? I would say, not much but I can't point to any specific supporting experiment, so, it's just my opinion.

Could a disease be brought back via this kind of research?

Hardly. Lot's of parameters (an overview here)  must be just right to have a virus spreading and cause disease. Viruses are usually very attuned to cells metabolism and environmental factors. Current parameters are probably very different from the original ones so, even if an ancient virus can be "revived", its ability to infect and spread would definitely be hindered.

Or are the conditions for waking latent viruses from starting material of this
  kind just not possible to recreate in a lab setting?

There are no standard conditions to awaken a dormant virus, or in general to produce viruses. Each virus is different and it will require specific conditions (here some examples on Lentivirus and Adenovirus). In theory, if all the required viral proteins can be expressed in a compatible cell host, then viable viral particles can be produced (Negev virus, Rhopalosiphum padi virus, Black queen-cell virus). "Reviving" an ancient virus is definitely possible with enough effort, but again, the rate of success will differ from virus to virus.


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DNA as a digital storage medium; sequences algorithmically avoided for safety reasons (or should be)?
Safety for the environment is probably implicit here as well, but the focus should be on the people who may come in contact with large amounts of synthetic DNA used to encode information as a data storage medium.

The idea of using DNA as a digital storage medium is not new. Two papers are listed below but there are many others.
Recently the concept has been further highlighted by the news of a "movie" being encoded using CRISPR-Cas. A Harvard University video explains the process:

In this video, Wyss Institute and Harvard Medical School researchers George Church and Seth Shipman explain how they engineered a new CRISPR system-based technology that enables the chronological recording of digital information, like that representing still and moving images, in living bacteria. Credit: Wyss Institute at Harvard University
For more information, please visit: https://wyss.harvard.edu/taking-cells...

below: a GIF showing the original data, and the "movie" interpreted from the recording in DNA. From the Los Angeles Times:

DNA DVR? Scientists have uploaded a short movie of a galloping horse into the DNA of living bacteria and were able to retrieve it with a 90% success rate. (Seth Shipman)

The immediate application in the Harvard Wyss Institute work seems to be (based on my understanding of the video) in-situ data logging, where information relevant to an experiment is recorded in the DNA of cells involved in the experiment. So the use of a moving image is a way to bring home the key point of "chronological recording of digital information".
Other uses involve the DNA itself, stored outside of living cells, as simply a mass storage medium.
QUESTION: I'm wondering if there are sequences that are likely to become algorithmically avoided as standard practice for safety reasons (or should be) when using DNA as a digital storage medium. The DNA may be handled by IT personnel rather than trained biologists, or shipped, or otherwise not be treated with the same diligence to safety that synthetic DNA is handled by researchers today.
Some other discussions of DNA as a storage medium:
Next-Generation Digital Information Storage in DNA, Church, Gao, Kosari, 2012. doi:10.1126/science.1226355
Towards practical, high-capacity, low-maintenance information storage in synthesized DNA, Goldman et al. 2013. doi:10.1038/nature11875

For further background on the temporally encoded data work, see the excellent answers to the question What does it mean to “write an image and GIF into the DNA of bacteria”?
edit: I'll quote a comment here just to make sure that the word safety isn't misinterpreted as data integrity or the safety of the bacteria:

When speaking of safety issues related to the handling of biological or biomolecular samples, it's the safety of people that we worry about. Safety rules, safety procedures, safety courses, safety glasses, these are for the safety of the human, not the safety of the sample.

An identical or near-identical question to this has been posted before, but I can't find it, maybe it was deleted. Just a reminder in case anyone else can find it...

@BryanKrause There is a deleted question which was similar. Here I've used some of your helpful suggestions and also removed the less-relevant material which seems to have been distracting. However please don't assert that I must prove DNA is dangerous before I can ask if DNA would be treated with caution.

Oh okay that was your question. Do you have the paper you cited there? It might be the Church one you have here, that sounds familiar. I seem to recall that paper describing exactly this issue. I'm wondering what answer you are expecting beyond what they said.

@BryanKrause I seem to remember that there is one sentence in this one five year old paper. The field of molecular biology moves quickly, so that doesn't make it the last word on the subject going forward. Is there something about this question you find unsettling? Can you let it go for a day or two and see if some informative answers are posted? Possibly post one yourself? Stackexchange is about getting answers for ones self, but also the generation of answers that can be read by many.

I'll try to write an answer when I have more time, but the two answers here are examples of why I was asking you about Church. Neither of the writers of these answers seem to have read Church, because they are ignoring all of the issues that paper raises. If you included that information in your question and made clear what about those issues you are interested in, you would get better quality answers.

You might br interested in this

@another'Homosapien' Lots of goodies to read there - I'll add a reference to that in my question. Thanks!!

@another'Homosapien' thanks for the edit - looks better!

DNA data can theoretically be used as malware: http://dnasec.cs.washington.edu/

Yes, there could be sequences that a DNA based system could not store handle/very well: repetitive DNA sequences.
Not only do such sequences make a lot of problems during the sequencing ('reading of data'), but they are also more prone to form secondary structure elements like loops, since repetitive DNA can bind to itself in various different ways. This means that similar to natural occuring repeats they are more likely to mutate during DNA amplicifation (the number of 'copies' can quite easily change), which makes the 'data' more instable.
A possible way to solve this problem would be to use specialised data formats that avoid as much Repetition of data as possible (similar to how zip or jpg files work)
Otherwise I agree with Nathan, that DNA by itself is not dangerous (since it won't do anything outside of cells, and the bacteria used in molecular biology are generally harmless unless you start eating them in large quantities or otherwise getting them in your body). The possibility that the DNA could somehow code for toxic proteins is very very low, and you could just check that the 'data' in the DNA does not form a protein by chance anyway.

Have you read the discussion of safety issues in the paper the OP cites? This answer suggests you haven't. Biology.SE prefers researched and cited answers. Although you have a couple links in your answer, neither are directly related to the issue at hand.

Thanks for taking the time to post. You've actually answered an interesting question that I didn't ask but wish I did! I've asked about safety and you've discussed data integrity or stability, which is probably a more interesting topic.

Given the quantity of storage, with no avoidance system, you will eventually encode toxic or dangerous proteins.  But the system would have no molecular machinery to even transcribe it into proteins, let alone what may be necessary for proper secondary processing so that the protein would be active.  Now if they started somehow storing data into proteins as a final form, we'd have to be a lot more careful.

Data written on a discarded floppy disk (remember those?) or hard drive or thumb drive in a landfill has no hope of its data getting into the bacteria in the landfill, but the fate of data stored in DNA is less certain. In DNA written without safety rules, there may be sequences that bacteria or phages could find not necessarily toxic, but instead "very interesting" or even helpful. That's one random scenario.

Even if DNA drives (to give it a name) are being handled by IT professionals instead of trained biologists, we can still expect the environment to be clean enough so that no organism would tend to be affected by it. Also, as @nathan points out in the other answer, free DNA cannot do anything on its own. Its just like an open book, you can't get anything from it unless you have a reader (protein) for it. There have been no reports claiming that foriegn DNA (called cell-free DNA or cf-DNA for humans) has ever caused any health issues. In fact, there are no reports of cf-DNA even being transcribed by humans. You might also want to have a look at this to find out more. However, as pointed out by @AlanBoyd in comments, organisms residing inside humans can take up free floating DNA from their surroundings. For example, Heliobacter pylori has been shown by Stingl et al, 2009 to take up free DNA from its surroundings. Keeping that in mind, there are chances that DNA drives could be harmful (if, by chance, the drive contains some genes that might provide some antibiotic resistance to the pathogen). Some microbes show a phenomenon known as natural competence i.e. they simply take up plasmid DNA from their environment, break it into parts by restriction enzymes and add it into their genome. These organisms, which generally possess sex pilli for DNA take up, can be a major threat to the use of DNA drive if the users of DNA drives show carelesness while handling and mainpulating DNA since some of this DNA might provide them with antibiotic resistance or capability to infect humans. However, we can prevent this from happening by making sure there are no restriction enzyme recognition sites in the DNA of the drive, so that the organism cannot cut the DNA for ligation into its own genome.

This looks like the beginning of a fascinating answer! As I mentioned in this comment (and obliquely in this comment) sequences that might be avoided for data integrity might be a more interesting question, but I've asked about safety. Maybe you can divide these various items into data integrity and safety categories or somehow make it clear which would need to be avoided for reasons of safety?

@another'Homosapien' my understanding of the question is that DNA sequences created solely for data storage might inadvertently contain elements that are biologically unsafe - is this so, and what precautions would need to be taken to avoid this?

When talking about safety issues related to the handling of biological or biomolecular samples, it's the safety of the person that we worry about. Safety rules, safety procedures, safety courses, safety glasses, these are for the safety of the human, not the safety of the sample. There may be a bias that DNA is "safe" so the word must be talking about something else, and of course data integrity is more interesting and easier to answer. I can clone this question and re-ask specifically about safety, and change this one to data-integrity if it works with all the answers here, what do you think?

Or leave this as safety (and stress the human part more) and clone the question and make it about integrity and you can move the integrity part of your answer there. Whatever is most accommodating to those taking the time to post the answers.

Are you prepared to post an answer, citing recent authoritative sources that "...there are practically no dangers working with DNA drives"? Because this is what I'm asking, and I'd like to see how an answer like that fares - general agreement and lots of up votes or concerns and criticisms. I'm asking and looking for a proper SE answer, because I'm not sure, so I'd like to see perspectives from those more knowledgable than I, and then follow up by reading the linked sources.

It doesn't answer the question, it's an opinion. Do you understand why an answer of "I can't think of any related issues" is not an answer to a request for an authoritative source? You're saying that you think it's safe because you don't happen to know of a reason why it isn't. I'm looking for some scholarly work that addresses the safety issue as might be expected in an SE answer, and I've reinforced that again in my comment in the Bounty banner.

'none of the organisms that I know tend to just take up free DNA from their environment' many bacteria do this such as Helicobacter - see this paper for example

@alanboyd dude thats a very nice point 'bacteria inside humans could take up DNA'. I don't want to take the credit of this idea from you, but thanks a ton for that :D

Do you want me to post a separate question about data integrity where you can move the data integrity part of your answer and I there's some chance it will be the accepted answer?

So far you've really given me only stated your personal opinion regarding safety, and support your opinion with a few links on other topics and certainly not related to DNA synthesis for data storage. Then you have a much longer section which is unrelated to the question. This is not a good SE answer to my question.

Comments are not for extended discussion; this conversation has been moved to chat.

I'm wondering if there are sequences that are likely to become algorithmically avoided as standard practice for safety reasons (or should be) when using DNA as a digital storage medium.

I don't think the sequences themselves are the concern here, so much as the procedure used to integrate them into bacteria for data storage, which I don't think is of direct risk to humans.
In the Shipman-Church paper, video frame data are encoded into chunks that are 27 bases long, interrupted by short PAM spacers and barcodes to aid in resequencing (for time-directed data readout).
The larger 35-base oligonucleotides are administered into the host bacteria via electroporation — effectively shocking the cells, which opens up the cell membrane to allow the oligonucleotides to get in for the bacteria's existing Cas1/Cas2 system to integrate into the genome.
Electroporation can be used for delivering oligos in vitro, into human cell cultures, but not typically to live humans. Lab safety and contamination protocols are used to prevent exposure to reagents and limit risk of electrocution.
Even so, shocking people wouldn't be enough as the sequences themselves are not enough to be the risk. Efforts at CRISPR human gene editing in vivo typically focus on the Cas9 system. Human cells don't express Cas9, so that bacterial protein would have be delivered along with the target sequence, which would use delivery techniques not used in this paper (e.g., injection or lipid-based delivery).
It may even have to be done in such a way as to get around immunity to Cas9 protein, or be directed at stem cells or other cell-specific population to have a desired effect.
A 27-base sequence could theoretically target genes critical for health — say, deletion or insertion of some 27-base sequence within an oncogene or tumor suppressor gene, for example, delivered with the CRISPR-Cas9 platform. But to administer this, you'd need an entirely different protocol than what the Shipman-Church paper describes, in order for this storage medium to begin to create the possibility of a safety hazard for humans.

Going to the (paywalled) Goldman-Birney paper, they do not store their data in bacteria, but simply synthesize DNA oligonucleotide strings and effectively store them in blobs of fat (literally). When they want to do data retrieval, they do shotgun sequencing with high coverage to get back the original sequence.
As such, there is no real risk of incorporation into human cells, short of microinjection, and so no real direct risk from subsequences being transcribed and translated into pathogenic proteins or virus particles, etc.
While the sequence data could itself contain pathogens, your IT fellow would need to bring their own protein machinery and protocols to have anything nefarious happen. Sequencing is what is done to affect data retrieval, not transcription/translation, and sequencing does not activate any code in the underlying sequence.

I would say no for two reasons.
The first is I don't know of any DNA sequences that are in themselves infectious.  You'd need the proper cellular machinery to make anything out of them.  If I'm not mistaken even most prokaryotes have varied defenses against random pieces of DNA getting incorporated into their systems.  Otherwise they'd never have stable cores. Viruses and bacteria etc have to use strategies to get around those defense systems.
The second reason, even if I'm wrong on the first, is that this system must be designed to be as free as possible from outside influence.  A system designed to minimize external influence also inherently minimizes influence to the outside, at least in this case.
This wouldn't be handled by IT people unless it was somehow massively automated.  Again no clue on the final form, so hard to say.

Have you read the discussion of safety issues in the paper the OP cites? This answer suggests you haven't. Biology.SE prefers researched and cited answers.

Thanks for your thoughts. Infectious proteins took science by complete surprise decades ago, and it took a while for people to agree it was happening. However, as you point out, since DNA is primarily information, it probably doesn't have much ability to induce molecular changes on its own. Instead, it usually needs to be accepted into, or forced into a transcripting environment.

@uhoh Exactly.  If you've never tried to transfect e. coli in a lab, I can tell you that it is nontrivial, at least for an undergrad who only does it a couple of times.  I wasn't able to access the Nature paper so if there is a list of other safety concerns I did not consider, my apologies.  Infection was just the first thing that popped into my mind as far as safety.  I guess other than that I would think all the other safety issues would be related to standard DNA sequencing work, which is pretty well OSHA'd up.


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Modeling the production of mRNA
I have the following example of how an equation for the production of mRNA in a particular organism could look like:

Consider the following equation for the production of mRNA for a gene Y. Gene Y is expressed from a promoter that is repressed by protein R. For example, if Y is GFP above, then R would be TetR.
  $$
\beta_{Y m}=\left[\frac{\beta_{y \max }}{1+\left([R] /_{K_{R Y}}\right)}\right]
$$

And now I am trying to understand what the different variables of the equation are.
$\beta_{ymax}$ must be the maximum rate at which mRNA can be produced and $R$ is concentration of a repressing protein, but what must then $K_{RY}$ be? Is it as simple as that it is an inducer for the production of mRNA?

Where did you get the equation from?

At a first guess, $K_{RY}$ is a dissociation constant for the repressor binding of the gene Y promoter, but it's hard to say without more information. e.g. David's question. Also, it is best practice to reproduce the equation as text rather than as an image, to make it easier for screen readers.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your post accordingly. In particular, quotes and other copied material must be referenced — this is the standard practice in scientific communication and will also help other users understand the context for the quote. ———  In addition, it would be very poor writing if these terms were not all defined and explained in the accompanying text — please confirm that isn't true ... Thanks!


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What species are these juvenile birds?
What species are these juvenile birds found at São José dos Campos, Brazil?

A puppy is a young dog. There exist a number of correct terms for birds (chick, hatchling , nestling, fledgling and other species specific terms). See here for more information

@Remi.b Excuse me. I'm Brazilian and I wrote wrong.

@LCarvalho No worries. I make plenty of english mistakes myself. Can you please add the location where you took that picture?

From São José dos Campos

I am flattered by my question having had so much attention from reputed people. Well, I found the right site to ask. I did not expect it to be like this.


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Can someone please explain the following jargon to a layman
I was reading an article on a substance called apigenin:

Apigenin can inhibit both aromatase and 17β-hydroxysteroid dehydrogenase (17β-HSD) with the inhibition of 17β-HSD being unique to apigenin and 3 other tested flavonoids (chrysin, genistein and naringenin)[22] and apigenin possessing an IC50 of 300nM (0.3μM). The IC50 of Apigenin on aromatase is approximately 2.9μM (most potent tested flavonoid on aromatase was 7-Hydroxyflavone at 0.21uM, outperforming the reference aminoglutethimide at 1.2uM[22]) and both of these enzymes are involved in testosterone synthesis at different stages.

Does this mean that higher apigenin potentially yields higher or lower levels of testosterone? I guess I'm unsure what the implication of "inhibits" is.

As far as I can tell, aromatase is involved in the conversion of testosterone to estradiol, so it’s inhibition should increase testosterone. However, 17B-HSD is involved in testosterone biosynthesis and its inhibition should have the opposite effect. And there are potentially other pathways that it affects, so you’d probbaly need to find a paper that actually looks at testosterone levels in vivo.

So, to inhibit substance $A$ means to prevent it from reacting with anything else?

It's inhibiting enzymes, which prevents them from catalyzing their reaction(s).

So I can definitely explain what "inhibits" means and what that implies, but I think the answer as to what apigenin is actually doing to testosterone levels is somewhat complicated. I wasn't able to find a study looking at steroid levels in vivo following apigenin administration, so this is based solely on a quick look through the biochemistry and cells biology available.
17β-HSD is an enzyme that catalyzes a reaction (meaning it makes the chemical reaction happen more quickly than it would by itself) that converts androstenedione to testosterone. If it is inhibited, that means that the enzyme is no longer able to catalyze the reaction. Therefore, inhibition of this enzyme should prevent the synthesis testosterone, and reduce its levels, since less testosterone will be made.
On the other hand, aromatase is an enzyme that converts androgens, namely testosterone and its aforementioned precursor androstenedione, into estrogens. So, one would expect inhibition of this enzyme to lead to increased testosterone levels, as less testosterone and androstenedione would be converted to estrogens, meaning more testosterone and its precursor are left unchanged.
So, it seems we have some competing actions. Based on the paragraph in your question, apigenin's IC50 for 17β-HSD is 0.3 μM, and its IC50 for aromatase is about 2.9 μM. That means that when the concentration of apigenin is 0.3  μM, the enzyme activity of 17β-HSD is cut in half, but it must be at a concentration of 2.9 μM to do the same to aromatse's activity. So, it is about ten-fold more potent at inhibiting 17β-HSD than aromatase, at least in the assays used above. That would suggest that at concentrations significantly below 2.9 μM, apigenin would inhibit 17β-HSD but not aromatase, resulting in a decrease in testosterone. However, once concentrations became sufficiently high to allow for inhibition of both enzymes, things would get more complicated. Depending on the relative amounts of both enzymes, how much access apigenin was able to get to each, and what the cellular steroid composition was prior to inhibition, you could imagine relative testosterone levels to go either up or down. However, I would be inclined to suspect that testosterone levels would in fact decrease in the long run, since eventually existing testosterone stores would be depleted, and the inhibition of 17β-HSD would prevent the creation of new testosterone.
However, if we look at the paragraph in the article immediately following the one you quoted, there is a summary of a study done in cells that found that apigenin actually increased testosterone levels by blocking the TBXA2 receptor. This inhibited a signaling cascade that normally decreases testosterone synthesis, so the end result was an increase in steroidogenesis/testosterone production.
So, I suspect things are actually somewhat complicated and the best way to know would be to test in vivo


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Link between pornography abstinence and hormone levels
I have a question regarding abstinence from pornography, and also possibly celibacy, and how these two lifestyle choices affect hormone levels.
Trends such as No Fap have been emerging recently. An excerpt from their website states :

No Fap held you to sharply increase your testosterone levels.

Is this true? From my research, I see no evidence to suggest this. Links to any studies would be appreciated. It is clear that people participating in No Fap have experienced psychological changes, but whether these changes are present on a hormonal level is an interesting proposition. If there is no hormonal change, what does this infer about what has happened to the minds of participants?

My immediate response, although I have zero evidence to back this up, would be it's along similar lines to quitting eating chocolate. You're simply stopping a habit that you enjoy. It sucks at first but then you get used to it after a period of time. More likely to be to do with dopamine than anything else.

Thanks for your answer. Yes, after doing more research it would seem that a pornography addiction desensitises the dopamine receptors in the brain and hence affects the wellbeing of the person in other activities. I suppose this could have the same kind of effect as low testosterone or adrenaline does.

I've written this up for you as a proper answer, if this solves your query I'd appreciate it if you marked it as accepted

In the context of breaking a pleasure producing habit, such as masturbation (with or without pornography), testosterone plays very little part.
There are two factors at play here:

Habitualisation - the tendency for an orgasm to repeat behaviours that it has become accustomed to.
Addiction/Dopamine Response - it feels good so I'm going to carry on.

The first bullet point is obvious, if you've always done something, it's going to make you feel different if you stop. If generally in society it is perceived as being a bad thing (thus making you feel guilty for partaking, even subconsciously), stopping that habit will make you feel good. Especially once you've gotten over the relapse stage.
The second bullet point is more involved. Orgasms, along with the viewing of sexually stimulating material, release dopamine into the blood. Over time, the dopamine receptors in the brain become desensitised and require more and more dopamine to get the same buzz. This is exactly why drug addicts need bigger and bigger doses of their drug. Consequently, once one has stopped partaking in the dopamine producing behaviour the receptors gradually begin to return to normal levels of sensitivity. This results in a generally better mood and a potentially higher libido. To those that don't know the root cause, this increase in mood and libido may appear as though testosterone levels had increased, however, this is likely not the case.


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How to evaluate broad-sense heritability of microbiome associated plant genotypes in R
I have a data containing 196 accessions of A. thaliana from which I studied leaf bacterial and fungal community and, therefore, sequenced and found several OTUs. Now, I want to evaluate broad-sense heritability of microbes across accessions of A. thaliana in R. Kindly reply and if needed, I'll provide the data table.

As a disclaimer i don't know how to do this, but a package exists in R for these calculations. The package contains datasets from Arabidopsis you can use to play around with the functions.

Can you explain what you mean by "evaluating the heritability"? Moreover, how to do something in R is not really on-topic here. The focus should be on the idea instead of the programming.


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What kind of spider is this? Brown with white spots

It was found in Houston, Texas, but I've never seen one before. Does anyone know what it is?

Your pictures are really small. Don't you have better ones? 2) You displayed twice the same picture. Why? 3) The fact that you were scared of this little creature and decided to offer it one of the worst possible death is up to your own standards in ethics but it is certainly not a necessary information to ID this species.

The fact that you killed it is irrelevant and apparently unsettling to some people. Stop putting it back in your question.

Sub-adult tropical orb weaver spider.  "Its range is largely circum-Caribbean, occurring in Florida, Louisiana, and Texas along the Gulf Coast of the United States."

Harmless to humans and considered beneficial.

Bites of this species are not known to cause serious effects to humans. ... The web probably catches many moths and other night flying insects; these spiders may be particularly beneficial along woodland borders of field agroecosystems and within orchards.


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What is the best solvent for Mutagen X?
Many solvents can be used for mutagen X (3-chloro-4-(dichloromethyl)-5-hydroxy-5H-furan-2-one), however, long-term stability is not specified. Which would be the best solvent for long-term storage? Once dissolved, can it be stored at RT or -20ºC?
Thanks


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Can DNA fingerprinting tell you if someone has been genetically engineered?
I am writing a fictional novel about an extensively genetically engineered man, unbeknownst to him, who gets into trouble on a regular basis. The man is physically large and strong, very fast (tiger-like hand speed), and he has exceptional sensibilities such as night vision, hearing and smell. The FBI gets some of his saliva from a crime scene and creates a DNA fingerprint from it.
My question/s is: could the technicians/scientists who perform the DNA fingerprinting procedure for the FBI be able to tell that this man is different from other humans? Would it be possible for someone to be human and have a different number of chromosomes? Does all DNA fingerprinting appear as bar codes and mean nothing until compared to a sample?
Please forgive my ignorance on the subject. Thank you for any input.
Chris

Can you clarify what you mean by "different from other humans"? I assume you mean could they tell he was super human, not just tell him apart from other people? If it's the latter then yes, since that's basically the point of fingerprinting.

You could try your question on WorldBuilding.SE, too. I'd expect there are some people there with a background in biology, at least enough to know some of these forensic techniques that are often of interest to the general public. There it would also be on-topic to ask in the style of "I want this to happen in my story, is this feasible?" for example, if you wanted a feasible way for your FBI to start to reveal the nature of this individual. @canadianer's example is about as far as we can go here without straying off topic.

Based on the answers below you could decide to have one or two  modifications that showed up as odd in the fingerprinting which leads to a whole genome sequence being determined. Especially if the story is set in the near future.

Could the technicians/scientists who perform the DNA fingerprinting procedure for the FBI be able to tell that this man is different from other humans?
If by different you mean genetically engineered, it depends on whether the loci tested have been engineered to such an extent that they are substantially different from other humans in order to arouse some kind of suspicion. There are other tests could be done that would show, at the least, that this individual's genome is abnormal.
Would it be possible for someone to be human and have a different number of chromosomes?
Yes, this is called aneuploidy and is the cause of many genetic disorders. Fingerprinting would not detect this.
Does all DNA fingerprinting appear as bar codes and mean nothing until compared to a sample?
DNA fingerprinting looks at sequence length polymorphisms and essentially tells you the length of certain regions of DNA in an individual. In fingerprinting, samples are compared to see whether DNA from two samples come from the same individual. A single sample obviously wouldn't work for this, but that doesn't mean it would tell you nothing.

Just to add, modern "fingerprinting" uses short tandem repeats that are (mostly) free of biological activity, so it seems unlikely that some engineered human would differ from his parents any more than their unmodified children would. And if there are new genes added on a new chromosome, well, those would be completely invisible to the technique unless it contained sufficient sequence similarity with one of the targeted STRs.

To answer the questions separately:
1 - "Could the scientists tell that this man is different from other humans?"
The functional basis of DNA fingerprinting, is to use regions of DNA that are known to be highly variable between individuals, such as micro- and minisatellites (short, highly repetitive stretches of DNA).
This is explained in fairly basic terminology on the wikipedia page for the topic.
As such, if your question means "can this be used to distinguish him from other people", then the answer is yes, absolutely. That's exactly why DNA fingerprinting is used in criminal trials etc.
If the question is "could the stretches of DNA used in the fingerprinting procedure show if someone is 'super-human'" then there are 2 issues I can think of:
The first is up to you:
You have the creative freedom to decide where in his DNA these alterations have been made. If the modifications are not in the areas that DNA fingerprinting would test, then no.
Since the modifications that would give marked phenotypic changes such as sight improvement etc. are likely to need be in coding DNA sequences (the ones that typically give rise to proteins, though this is an exceedingly loose definition), it's probably pretty implausible you'd be changing regions DNA fingerprinting examines. Tandem repeats dont generally have well known or defined biological roles. They're often referred to as 'junk DNA'. Though this term is falling out of favour as we're beginning to realise there are more subtleties to genome architecture.
Secondly, if we assume you do elect to modify some satellite sites, it would be extremely unlikely that this could ever be linked to 'super human' phenotypes. Determining whether or not a mutation, even in a coding sequence, where you can examine the protein product and the organism experimentally, has any biological effect, is still extremely hard to do. Not to mention, a vanishingly small number of spontaneous mutations in a sequence ever give rise to an 'improved' sequence.
2 -"Would it be possible for someone to be human and have a different number of chromosomes?"
Absolutely, this is a well documented condition, generally called aneuploidy. 'Ploidy' is the fancy term for chromosome copy number.
Down syndrome, AKA "Trisomy 21" is probably the most well known example of this. Sufferers are very definitely still human. As the scientific name implies, they have 3 copies (so 1 additional) of chromosome 21. It is also possible to be lacking chromosomes, as well as having additional copies (for example, Turner Syndrome.
3 -  "Does all DNA fingerprinting appear as bar codes and mean nothing until compared to a sample?"
Generally yes, you'd compare 2 samples to obtain an answer. You perform fingerprinting and sequence length polymorphism studies on your 'subject' sample, and on your 'reference' sample, and if they have the same banding pattern, you have a match. It will still contain information though. Those samples could be sent for sequencing for instance, which would tell you to even greater resolution, how similar 2 samples are.
EDIT
Just as a final thought (though getting a bit off the scope of the SE), if you did want the authorities to be able to tell that someone had been genetically modified, you could propose that those microsatellites are changed to something non-repetitive, which would potentially stand out. Or go even further and 'watermark' the genome, much like Venter et. al did, with the first synthetic genome (they incorporated a code to spell out messages in 'junk' regions of the genome).

Adding to what the two other answers have said, normal DNA fingerprinting tests do not tell the researcher how many chromosomes the organism has. That is part of a different process called karyotyping. However, karyotyping is actually surprisingly low-tech, people have been karyotyping for years before genetic sequencing was even a thing. That said, it is unlikely a researcher would think to look for karyotyping unless there was some evidence the subject suffered from a chromosomal disorder like Downs' syndrome or Turner syndrome.