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Flora and fauna of early homo sapiens environment?
Where can I find as much detail as possible on the flora and fauna (and perhaps geological structures too) between the time of the origin of Homo Sapiens say ~300kya to their "out of Africa" migration?
I haven't been able to find much research on the topic. I am looking for the types of predators they would have had, the foods they would have eaten, the plants and animals and bugs they would have encountered, etc.. If at all possible.
To put it another way, what are the flora and fauna of the Great Rift Valley.
https://en.wikipedia.org/wiki/Ethiopian_Highlands#Ecology

It's a bit outdated, but Quézel (1978) suggests the flora of the Mediterranean region of Africa is not much different than today:

It is concluded that the Mediterranean flora is relatively old and goes back at least as far as the middle Miocene

See here for a scale of Geologic time. The middle Miocene would be ~10mya, so the above quote encompasses your time of interest.

However, I personally find this claim to be difficult to believe, especially due to documented variability at smaller scales: (e.g., Moreau 1963, Carlo et al 2009, etc.)
Other literature, unsurprisingly, points toward the fact that humans very likely modified their surroundings in noteworthy ways once on the scene. For example, Thompson et al. 2021:

Archaeological data and principal coordinates analysis indicate that early anthropogenic fire relaxed seasonal constraints on ignitions, influencing vegetation composition and erosion. This operated in tandem with climate-driven changes in precipitation to culminate in an ecological transition to an early, pre-agricultural anthropogenic landscape

Perhaps Gardner (1935) would also be of interest (I don't know, I don't have access).
Conclusion: I don't know the answer and only compiled the above in about 5 minutes of Google Scholar searching. I would guess that both the flora and fauna were likely somewhat dynamic across the time period you're asking about, and certainly, spatial physiognomic heterogeneity exists even today.
To narrow further searching, make sure you're using technical terminology where possible (e.g., late Pleistocene, Chibanian, etc.).

Citations:
 Carto, S.L., Weaver, A.J., Hetherington, R., Lam, Y. and Wiebe, E.C., 2009. Out of Africa and into an ice age: on the role of global climate change in the late Pleistocene migration of early modern humans out of Africa. Journal of human evolution, 56(2), pp.139-151.
 Gardner, E.W., 1935. The Pleistocene fauna and flora of Kharga Oasis, Egypt. Quarterly Journal of the Geological Society, 91(1-4), pp.479-518.
 Moreau, R.E., 1963, September. Vicissitudes of the African biomes in the late Pleistocene. In Proceedings of the Zoological Society of London (Vol. 141, No. 2, pp. 395-421). Oxford, UK: Blackwell Publishing Ltd.
 Quézel, P., 1978. Analysis of the flora of Mediterranean and Saharan Africa. Annals of the Missouri Botanical Garden, pp.479-534.
 Thompson, J.C., Wright, D.K., Ivory, S.J., Choi, J.H., Nightingale, S., Mackay, A., Schilt, F., Otárola-Castillo, E., Mercader, J., Forman, S.L. and Pietsch, T., 2021. Early human impacts and ecosystem reorganization in southern-central Africa. Science Advances, 7(19), p.eabf9776.

Early human migrations may have gone through Yemen. The Red Sea rift has become salt flats multiple times because of the ice age, if you find studies of the salt strata please write a new answer.
The science keywords are Pleistocene fauna, flora and Pleistocene ecology.
There were a lot more species/varieties of elephants, hippos, homo, deer, zebra, birds, bears, felines, with large mammal species enduring 1+ million average roughly depending on taxonomic precision. The plants were 90% the same, and plants can move roughly 100km to 10,000km per 1000 years conditions permitting. The green zones moved in a patchwork mosaic that was also tended by herbivores and dependent on climate. Tree species also change in more than 1+ million year ranges, perhaps 5-20, I don't know.
The mountains change yearly by 1cm for granite, 1-10cm limestone 10-50cm flysh and schist, 10-100cm for chalk, and 1+ meters for unconsolidated volcanic. The major changes were therefore climate changes
The rift valley is 5500km long, so It's too complicated to answer.
Here's animals from the holocene:
https://en.wikipedia.org/wiki/List_of_African_animals_extinct_in_the_Holocene
Here's some info about pleistocene, it's not very a very good list though, best to look at other sources.
https://en.wikipedia.org/wiki/Pleistocene_megafauna#:~:text=Pleistocene%20megafauna%20include%20the%20straight,and%20the%20leopard%20in%20Europe.


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Where can I find the standard curves for Bovine Serum Albumin (BSA) and ovalbumin as determined through the Bradford Assay?
I was wondering if anyone would please be able to point me in the direction of a database or something similar which contains standard curves/absorbance levels for BSA and ovalbumin, as measured using a spectrophotometer at 595nm, with the Bradford Assay?
Thank you in advance!

Really, you should make your own standard curve, as the concentration of your Bradford reagent may be slightly different than mine, or the one used in a paper, and spectrophotometers can vary significantly. Typically an ampule of BSA or OVA at a defined concentration in PBS is included with Bradford assay kits. This can be serially diluted, then duplicate or triplicate samples added to the same plate as your samples. You can also (very carefully) make standards yourself - just be sure to agitate them long enough so that the protein is completely dissolved.

Figure 1. Absorbance of Bovine Serum Albumin (BSA) at concentrations of 0, 40, 80, 120, 160, and 200 μg/μl at 595nm.
or
Figure 2. BSA Standard Curve with absorbance measured at 595 nm, a linear regression was deduced with equation of y = 0.0127x.
or
Steps 7, 15 and 16 here
or ideally
Please just use a search engine and type in "bradford protein assay 595nm bsa" or substitute "bsa" for "ovalbumin" and see what the world has made available for you in the realms of protein spectrophotometry at 595 nm.

That’s amazing! Thank you so much!

source: Stack Exchange

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

sort: votes


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What is the oxygen concentration in the lumen of the small intestine?
I am researching how oxygen affects enzyme activity in the small intestine, and I need to know how much oxygen there is in the lumen. I understand that the average amount of O2 in the lumen is ~2% (<10 mmHg), however I am curious as to how the number changes from the beginning of the small intestine to the end. If you were to measure O2 concentration from the beginning to end, would it be a decreasing linear or exponential curve.

From a recent review by Konjar et al. (2021), see Figure 2 and associated text:

There is also a steep decrease in oxygen longitudinally from the small intestine towards the colon.

Longitudinally—from the small intestine to the colon—the oxygen level
drops (Figure 2) [15,16], and a negative gradient is also observed
from lamina propria towards the lumen. To illustrate this, in mice,
pO2 drops from 58 mmHg in the stomach to 32 mmHg in the duodenum,
through 11 mmHg in the ascending column and to 3 mmHg in the sigmoid
column (all values measured using electron paramagnetic resonance,
EPR) [16].

For your convenience, I link references 15 and 16, respectively.

Although this is helpful, the values are taken from experiments done on mice. I am interested in the human small intestine.

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


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Identifying fish or shark jaw bone
I found this on the beach of coastal southern Maine in early March. The teeth are not a single row and lighter is for size comparison


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Does cytoplasmic streaming cause passive organelle movement in animal or fungi cells?
In plant cels there is a current debate about whether or not cytoplasmic streaming, which is thought to be driven by the force of myosin motors transporting cargo along actin filaments, can cause organelles to move by passive advection.
I want to know if this is a genuine means of transport in other eukaryotic kingdoms, and not just passive movement of small molecules, but actual organelles?

I believe that fungi use cytoplasmic streaming to transport organelles to the tips of their hyphae to extend them. I haven't heard of cytoplasmic streaming in animal cells but it might exist.

If you look at
http://en.wikipedia.org/wiki/Melanosome
you will see an example of this organelle being transported in animal cells.
Is this what you mean? or are you looking for unbound organelles being swept along by a current?

Thank you for answering, and yes I mean unbound organelles.


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What determines the color of the air sac of a Portuguese man o' war?
I know that the Portuguese man o' war is a colonial organism composed of many "zooids", one of which is the pneumatophore, which essentially serves as a flotation device for the whole colony. This sac may be of varying shades of pink, violet, or blue.
I'm having trouble finding a reference on how a particular man o' war gets its sac coloration. The most obvious possibilities are trace chemicals in the air and/or water or heritable genetic factors, but I'm not finding any sources.
What determines the color of the pneumatophore sac of a Portuguese man o' war? Is it genetic, analogous to eye color or hair color in mammals? Is it essentially dyed by exposure to various chemicals in the environment? Is it gender-based? Is there some other explanation as to why one man o' war might be blue while another is pink?


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What is the cause for these patterns on my kiwi fruit?

Have a look at the top right side of the fruit. There are these grid like vellular patterns over it. The fruit seemed tender at time of taking the photo.
Unsure if the pattern developed over ripening or not. Never paid attention except when I took it out of the bag.

It looks like a giraffe pattern: https://www.google.com/search?q=voronoi+in+nature&sxsrf=AJOqlzUHKjvL203Q28o9-8-PQ5bHU_sXVA:1679211970845&source=lnms&tbm=isch&sa=X&ved=2ahUKEwjW-5iIwOf9AhXqVqQEHZcnAf4Q_AUoAXoECAEQAw&biw=1707&bih=863&dpr=1.5

These are blemishes from rubbing of the fruit while on the vine (against other fruit or a branch) or possibly from damage from water sitting on the skin or from a mite or similar parasite.
There should be no or very minor damage below the skin on the part of the fruit that you eat.

That pattern is called a voronoi it corresponds to cellular shrinkage boundaries, like mud-cracks, giraffe patterns, puff balls, jackfruit skin, cell mushoom pores, fly wing veins, leaf cells, bubble cross sections, skin cells, and it can be found on interactive graphics like https://www.google.com/search?q=shadertoy+voronoi&sxsrf=AJOqlzVOpCKLmiwgEsDk2lcZzMhurWRgAw:1679212442864&source=lnms&tbm=isch&sa=X&ved=2ahUKEwiq5aLpwef9AhW6T6QEHVx5C7oQ_AUoAXoECAEQAw&biw=1707&bih=863&dpr=1.5

@bandybabboon you should write your own answer, perhaps citing this one, but giving some more background on Voronoi patterns in nature - how and why they form.


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choosing the right housekeeping gene for Western Blotting analysis for liver lysates
B- actin is used a great deal for quantitation of liver lysates. What other alternatives are there for WB analysis? should we opt for GAPDH or tubulin?

This is totally up to you, and the antibodies you have on hand. The quality of the antibodies helps as well. There are many so-called "housekeeping" genes whose expression is not necessarily greatly affected by various conditions. Beta-actin, alpha- and beta-tubulin, GAPDH, COX IV, Histone H3... all work well, and some are better in some scenarios than others. For example, H3 would likely be a much better loading control for nuclear lysates than actin or tubulin (even though both do occur in the nucleus in some circumstances), due to its much higher and more stable expression.

So, test what you have, and ensure that it truly isn't affected by your treatment or disease conditions. Also, make sure that the signal isn't saturated, otherwise you can't quantitate results and draw meaningful conclusions about your data.

I'm not posting an answer as I've voted to close this question as opinion-based. This is not a discussion forum; rather it is a Q&A site for biology researchers, academics, and students where specific objective questions relating to biology get specific objective answers. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question.

@MattDMo, I think there's an objective answer to the question "What other alternatives are there for WB analysis? ".

Use a total protein stain. Irrespective of tissue type, normalising your immunoblot signal using a total protein stain is a good, probably superior, approach (ref1, ref2, ref3). Many journal guidelines now strongly encourage the practice;

Normalize signal intensity to total protein loading (assessed by
staining membranes for total protein) whenever possible.
“House-keeping” proteins should not be used for normalization without
evidence that the experimental manipulations do not affect expression.

If you really need to use single protein loading control, confirm that it's stable in your hands; the abundance of any given protein in a tissue could still be perturbed by your experimental conditions.
Confirming consistent loading of your lanes using a total protein stain can help to confirm that your loading control is consistent in your experiment. I generally collect both total protein signal and a loading control but will only use the latter if a reviewer is being difficult.


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Is there a way to lyse bacteriophage with just heat?
I basically want the virus to fall apart into pieces. I want the capsid proteins to separate from the tail proteins and the DNA to all tumble out. I want all of the virus proteins, structural and DNA, simply to disassemble. If this were bacteria, I'd just use the freeze-thaw process to cause the bacteria to spill its contents into the solution it was suspended int. But apparently freeze-thaw doesn't work with viruses(?). Is there a way to do this by heating them up to a certain temperature? It is acceptable if there is a risk of proteins denaturing.

What is your end goal? What are you going to be doing with the lysed phages?

@MattDMo  I want to know if nothing more than bacterial cytoplasm proteins, Brownian motion, and time (and perhaps some ATP) are all that are needed for viral fragments and viral DNA to spontaneously assemble in an aqueous solution into complete and active viruses.

What happens when you research bacteriophage self-assembly?

@bob1 Thank you but I am not talking about self assembly of virion-like particles, or a hybrid mixture of some virus-like particles and other particles, or involving a functioning host cell.  I want to see if the assembly of the entire native virus (at least for non-enveloped viruses) can happen in vitro completely outside of a host cell, just in solution.

@edmundshelto yes... bacteriophage vlp then! What I'm suggesting you do is look at the literature and tell us what others have done, what they found, and what you plan to do. "Which Phage?" is a big part of this. This is part of the homework requirement.

the capsids of some phage, like HK97, are cross-linked and won't disassemble even if you boil them.

Of the five most common bacteriophages that live in the dirt in my part of the country, though they are all genetically quite different, all of them fall into the same general bucket as far as what temperature to use, and for what length of time. The capsomers will begin to denature at temperatures above 50-60°C (122-140°F) and can fully denature at temperatures above 70-80°C (158-176°F). The timescale is in minutes. That is about as specific an answer as I can get after extensive googling. All I can do now is collect samples, create lawns on TSA plates, isolate strains, pick plaques if and when they appear, denature the plaques at different times and temperatures within the parameters mentioned above, and test to see exactly when and at what temperature the cooked plaques fail to inoculate other colonies.


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How did birds reduce their tail and fuse the last caudual vertebrae into a pygostyle?
I was just looking at the phylogeny of Avialae and saw that birds go from having long tails made up of many caudal vertebrae (ex: Archaeopteryx, Jixiangornis, Jeholornis) to ones with very few vertebrae and a fused pygostyle (ex: Confuciusornithids, Chongmingia, the opposite birds, etc). Has anyone figured out what mutations caused this to happen?

have you tried googling pygostyle genetics, because I got a lot of good hits with just that.  I am not saying this to be rude but because questions like this are expected to show some attempt to research an answer yourself before asking for help. It is part of the homework question rule. Hint: something like it has evolved in more than just birds.


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Cellular respiration and membrane surface protons
The final product of cellular respiration is the proton motive force, formed by protons pumped out of the membrane and by the voltage due to all charges. While Mitchell’s original theory considered pumped protons released immediately to the bulk external medium, that has been criticized. Today there is a good amount of research showing that protons tend to remain confined in 2D in proximity with the membrane (one review can be found here). This would explain how certain extremophiles can survive in very basic niches (poor in protons), where the proton motive force, defined from the bulk pH, cannot sustain ATP synthesis.
As far as I have been able to discover, the existence of such “surface protons” has only been shown in vitro (e.g. in a sustained lipid bilayer).
Is there any experimental evidence of such “surface protons” in intact cells, i.e. in vivo?

I have take the liberty to edit question (you can always revert it if you disagree) to give it more focus. I particularly dislike questions asking for the "consensus in the field", and this is not necessary — all that will serve is evidence, and that is assumed to include citations. Remember, at one time the consensus here was squiggle-X! In fact, this is a biophysics question, although of considerable interest, I think is likely beyond the scope of all but one or two of the members of this list. You are probably as well doing your own search for papers citing the one you mentioned.


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What is the difference between monoclonal and polyclonal antibodies?
I'm having trouble to see a difference between monoclonal and polyclonal antibodies. The way I understand it:

Monoclonal antibodies are produced by the same "clone" or "line" of B-cells and, thus, can bind to a single epitope for some antigen.
Polyclonal antibodies are produced by multiple "clones" or "lines" of B-cells and, thus, can bind to different epitopes for the same antigen.

However, it is also my understanding that:

Every B-cell can produce only one kind of antibodies; i.e., the antibody molecules produced by an individual B-cell can all bind to only one epitope.

And so, when combining all these concepts, I can't really find any fundamental difference between monoclonal and polyclonal antibodies. To me, the distinction is only applicable when one is discribing the composition of a given substance (i.e. if such a substance contains Abs produced by a single line of B-cells or by multiple lines), but otherwise there's no difference between an individual "monoclonal" Ab molecule and an individual "polyclonal" Ab molecule; i.e., they'd both have the same general properties and functions.
I'd like to know if there is something I'm misunderstanding or if there's some information I'm missing.

I'd recommend looking into VDJ recombination to learn more about the underlying means by which antibody specificity / identity is defined. A clone of mature B cells derives from a single recombination event.

Welcome to SE Biology. Please do us the courtesy of finishing the [Tour] and then read the Help on asking questions, from which you will see that we require you to show the research you have done before posting. Wikipedia and a hundred other sites on the web explain the difference between monoclonal and polyclonal antibodies.  Read them carefully.

@David I'm aware that there are many sites on the Internet that explain the differences between these concepts, but I just like posting questions publicly so that fellow humans can condenscendingly and unhelpfuly answer to them. I also believe that I've clearly summerized in my question all the relevant information I've gathered so far from what I've read; please do me the courtesy of reading my question carefully. Thank you.

On reflection, I think that a lot of this question comes down to the meaning of the word "clone". Re: David's note about triviality, it is only trivial if you have a very clear idea of what this word means, as the root of polyclonal (many clones) vs. monoclonal (one clone).

Let me start again. You write "I'd like to know if there is something I'm misunderstanding". The answer is yes. You are thinking that the term "monoclonal antibody" is a description of an individual protein molecule, and implies that that individual protein molecule is chemically or structurally different from an individual protein molecule designated "polyclonal antibody". Antibodies are important tools in biological research, and for which they are generated artificially. Polyclonal and monoclonal refers to the heterogeneity or otherwise of the generated populations…

(cont)…So, as many accounts make clear, the key thing about monoclonal antibodies is that they are preparations (mixtures) in which all antibodies are identical in amino acid sequence (and which can continue to be generated to sustain research). This homogeneity of monoclonal antibody preparations allows applications/uses that are not possible with polyclonal antibodies, in which the individual molecules, although binding to the same epitope, have different aa sequences (and affinities and specificities). The applications/uses of monoclonals are many, and are amply described in the literature.

Monoclonal antibodies are like having a bag of tennis balls. They're all tennis balls.
Polyclonal antibodies are like having a bag of sports balls. If some of them are tennis balls, yes, they're the same as the monoclonal antibody tennis balls. But, the polyclonal antibody bag also contains baseballs and ping pong balls and basketballs. And there are far more possibly antibodies than there are sports balls, so it's most likely that your sports ball bag of antibodies doesn't have any tennis balls or any other specific ball you'd have thought of ahead of time, rather just a bunch of things that vaguely serve the purpose of being ball-like.
So yes, you're right, for an individual antibody, it's the same substance whether it's in a bag with only other identical antibodies or if it's in a bag with a bunch of other antibodies, but it still matters whether you have a bag of one antibody type versus a bag of lots of antibody types. The former is more standardized, you "get what you get" and it always will work the same; the latter is more diverse and binds multiple targets which in some sense makes it more robust (e.g., a small change in the target may prevent binding with one clone but not other clones).
Production is also different. Simplifying things a bit, for monoclonal antibodies, you produce the antibodies by isolating an antibody-producing cell and making lots of copies of that cell to make lots of that same antibody. There can be some variation in production but generally they are thought of as "one antibody".
For polyclonal antibodies, you inject an animal with an antigen, and collect the antibodies that are produced. You expect to get different specific antibodies each time, the only thing standardized is the antigen presented. (you can also do this with cell culture like monoclonal antibodies, except using a culture derived from lots of different cells)

I'd add an important distinction is often that monoclonal Abs have often only been presented with a short fragments which is approximately the length of an epitope, whereas polyclonal have often been given larger fragments or even full-length proteins to target, resulting in a diversity of epitopes.

@Bryan Krause Thank you for your easily digestable explanation. I was wondering, if there was maybe genetic factors that would make monoclonal and polyclonal Ab molecules different in some small but important way (like differences in their binding sites or in their backbone structures).

@OldCrow No, it's all in the name: mono-clonal "one clone", poly-clonal "more than one clone", where "clone" means "line of antibody-producing cells".


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Has a bird ever been seen stalling?
Note: I am not sure this is the right site, but I believe birds are off-topic on Aviation SE.

Has a bird of any species ever been seen experiencing an aerodynamic stall by increasing the angle of attack (AoA) over its wings or flying at too low of an airspeed?

I suppose you could technically call a dive a "stall". Watch a predatory bird stalking prey sometime. Once they're ready to attack, some species will just fold in their wings and let gravity do its thing for a time.

@MattDMo so when they do that they have no lift because their wings are folded in?

For a while, yes. They're in full control of the dive, so they can change direction using their tail if necessary, and can unfurl their wings to adjust speed whenever they want. It's not uncontrolled, just unpowered. On the other hand, there are birds that do power dives - flapping while diving. Here is an eagle doing just that.

And here is a blue-footed booby diving with wings folded.

Where have you looked for an answer to this question? Because basically stall is the mechanism by which many birds land on a perch.

Somewhat related

@kmm searching for "bird aerodynamic stall" just brought up things about the aerodynamics of birds (not stalling), aerodynamic stalls in airplanes, and explanations of why birds don't usually stall.

Yes.
Kereru (Hemiphaga novaeseelandiae) from New Zealand do a type of display flying where they deliberately induce a stall by flying on an upwards curve and allowing momentum loss to decrease air-speed such that they stall.
A video of this can be found linked through iNaturalist on Youtube.

Kereru were my first thought too. Nice work finding a video, they often fly to a decent height before stalling. So great to watch them on a windy day.


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How to name this bacterial gene when running out of letters?
There's a gene in some bacteria that I have to name.
My (very limited) understanding is that for bacteria, naming conventions are based a lot on Demerec et al. 1966 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1211113/pdf/61.pdf). Essentially, the point is to have a group of three letters designating a pathway or process (e.g. abc) and an additional uppercase letter identifying individual genes in a pathway (e.g. abcA, abcB, abcC...). Different alleles would be given numbers (abcA1, abcA2...). No Greek letters, superscripts, etc.
Now my problem is that for my pathway (let's call it abc) basically everything from abcA to abcZ exists already (some only in eukaryotes, and some were later proven to not be actually part of the abc pathway, but I think it would be confusing if I repeat those with a totally different gene).
I was initially thinking about using a Greek letter for it, but that's not allowed.
Does anyone know what is usually done when running out of alphabet? Thank you for your time!

I would guess that as you have an alphanumeric code already set for the pathway, using abc as the pathway name and A as the initial with alleles as numerics; that you would add an additional capital letter e.g. abcAA.

@bob1 Not unreasonable, but I wonder if it has ever been done.

I favour the suggestion from @bob1. It's up to you to see if it has ever been done. I had a quick go myself, but it needs some effort as on GenBank genes tend just to be numbered. What I would try is Streptomyces coelicolor and related strains, which are known to make complex antibiotics, or other bacteria which can make exotic molecules. Good luck!


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What is the purposes of these sugars?
What is the function of $\alpha$-D-glucofuranose and $\beta$-D-glucofuranose?
Are they both converted into energy? Or are they just different variations with no particular difference in function?
I tried searching but found nothing on the web except chemical structures.

What do you mean by purpose or function?

You see, there are types of glucose. And I want to know what a-d-glucofuranose and b-d-glucofuranose does in the cell.

I think you can ask that without referring to purpose or function, as these imply that  someone designed it that way versus being sort of an organic chemistry curiosity about glucose.

Please provide some context and describe the results of your own research. Why do you want to know about these compounds? Where have you read about them? Do they occur in the certain foodstuffs — or have you just seen their names in a chemical classification of sugars, and have no idea whether or not they occur in nature? I find nothing on the web except chemical structures.

So whats the problem about this question?

What makes you think they're found in cells? There are lots of things that turn-up in a biochem. lab which aren't found in nature, but are used in synthesis. Or just held onto for future use.

So are these found in cells of living things or not? Im very confused just give me the answer "they arent found in living things"

As a new user to this site "for biology researchers, academics, and students" you seem not to understand how this site or science works. You are supposed to post about a biological problem that you have encountered, and if anyone knows the answer they provide it with evidence or links to support. As far as I can tell — you still haven't told us — you have discovered a classification of sugars somewhere, and because glucose is a natural sugar you have assumed all other chemicals of this category are. This is not so, and chemists traditionally synthesize and describe any compound possible...

...You then ask us to tell you "they aren't found in living things", without understanding that we have no knowledge, evidence of other basis for saying that, so as scientists we cannot. The fact that we have never encountered them doesn't mean that some plant somewhere doesn't produce them. Chemists have synthesized thousands of compounds, so how should anyone here know which existe in nature (and why should we care)? We would assume that you would know something about them to go to the trouble of posting, but it seems not, or you are not going to tell us, so I suggest your post be removed.

Im sorry, im deleting this post.


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Total number unique chromosome combinations in fertilized egg?
Assume for this calculation no recombinations or crossover .
A male gamete (sperm) is haploid and has 23 chromosomes. These gametes can be selected from the father who has 2 pairs of 23 chromosomes each. So the total number of combinations for the male gamete is 2^23.
The female gamete (ie the egg) which is again haploid has the same number of total combinations 2^23;
These chromosomes are selected from the mother who has 2 pairs with 23 chromosomes per pair.
Thus the inital fertilized egg (ie one sperm plus one egg - ie diploid  ) I believe this means should have (2^23)^2 possible chromosome combinations. Is this correct ? This fertilized item would be diploid with 23 chromosomes in each pair; 23 chromosomes from the male gamete and 23 from the female gamete. Is my calculation for total combinations correct ?
Can one state that all these 46 chromosomes are always different? Ie for example the 2 chromosome #3 have a different DNA sequence ?

No. I suggest that you get a basic biology text book and look up chromosome pairing.

The fertilized egg is also called a zygote-ie the union of the male and female gametes.

Yes, and how does this apply to your question. You have some fundamental flaws in your logic!

@bob1 Seems reasonable to me, what am I missing?

There is no fundamental flaw; there are 2^46 possible chromosome combinations, excluding aneuploidy.

@BryanKrause The maths is right for combinations, but not about the last question, though there's some quibbling to be done there - is OP talking about the coding regions only? non-coding regions?

@bob1 I don't see much to quibble about regarding chromosomes being different; the chances of taking two Chromosome #3s from different people and finding them to be identical are sufficiently miniscule to ignore. Even from the same person it would be unlikely they're actually identical taken from two random cells.


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Recommendations for Books on Systematic Phylogenetics
I am a physics major and need to study systematic phylogenetics for a research project. Can someone please recommend at least one introductory and one advanced book, please?

What did you find when you searched online? Have you used Google Scholar or some other search engine like NCBI to look for review articles? What did you learn there, and where are the gaps in your understanding? As it stands, this question is opinion-based, which is off-topic on this site.

It would also be helpful to know what aspects of systematics you're interested in. Like, are you wanting to construct a tree? Are you comparing characters across species? Something else?

About which aspects of phylogenetics I'm interested in, mainly comparing characters across species and the methods for constructing trees, but since my knowledge is limited to Hennig's articles and a few youtube videos of a PhD in evolution, anything works, really.

I've managed to pick three books: [Joseph Felsenstein] Inferring Phylogenies, [Baum, David A.; Smith, Stacey D.] Tree Thinking - An Introduction to Phylogenetic Biology, and [Funk, K.A.; Brooks, Daniel R.] Phylogenetic Systematics as the Basis of Comparative Biology

Those books are probably a great start. I'm sure they cover it, but if you're comparing characters you'll need to be aware of phylogenetic comparative methods.


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Help to identify a odd skull
I found this skull in the woods, I came across an old stable that the roof was falling in. In the corner there was tree limbs stacked neatly as if something stacked them and the limbs were no bigger than a broomstick. The skull was laying on top of the ground not far from the neatly piled limbs.
I have google photo searched it in several different angles and found nothing similar.
I am at a loss as to what type of animal this could be. It is just very oddly Proportioned.
It does not resemble anything I have reached. Please help I identifying this skull.

I live in oklahoma by the way

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Welcome to the Outdoors SE. If you could provide photos for other angles and higher resolution for each, that would help with ID. You could also request migration to the Biology SE, which has ID tags too.

Also, would need some sense of scale - is this 2 inches or two feet long; can't tell from the photo.

It is 6 to 8 inches long

Very hard to say from the shape it is in.
Some observations:

The molars suggest it's a herbivore, the teeth look similar to what I know from the skulls of sheep/goats/roe/deer/...
Seems to have no signs of horns or antlers.
From the size I would say it is about the size of a roe/sheep/goat.

My best guess:
Since roe deer only live in Eurasia and not Oklahoma US I'd figure this skull could be from a small (young?) female deer or similar, or - if livestock is more likely - a variant of goat or sheep without horns.

I think White tailed deer juvenile or doe. No sign of antlers, teeth look right (curved row rather than straight) and cranium is about right too.


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semantical meaning of positions of letters in genomic sequences
here is a sequence from the human_nontata_promoters.zip dataset that represents a genome.
My question is whether the position in this genome data is consequent. For example, the positional letters at 0 to 10 are in charge of "this" from the position from 10 to 14 for another property.
TCCTGCCTTTCCACTTGCACCAGTTTTCCCACCCCAGCCTCAGGGCGGGGCTGCCTCGTCACTTGTCTCGGGGCAGATCTGCCCTACACACGTTAGCGCCGCGCGCAAAGCAGCCCCGCAGCACCCAGGCGCCTCCTGGCGGCGCCGCGAAGGGGCGGGGCTGTCGGCTGCGCGTTGTGCGCTGTCCCAGGTTGGAAACCAGTGCCCCAGGCGGCGAGGAGAGCGGTGCCTTGCAGGGATGCTGCGGGCGG
My knowledge in biology is almost zero and I would like to use this dataset for some purposes, I appreciate your help!

I would recommend thinking about DNA sequences more like words and sentences in a book than bits in a digital data file.
If you're reading a book and come across:

The quick brown fox jumps over the lazy dog

you don't need to know what character # in the book the sentence started at to interpret it. If you have another edition of the same book and you read:

The lazy brown fox jumps over the quick dog

you wouldn't say "oh, the 12th character used to be a 'w' but now it's an 'o'" (ignoring the spaces): that's true, but it's clear that the way these sequences actually differ is that two of the words got switched around. The rest of the sequence is the same, though, and much of the meaning is, too: there's still a fox jumping over a dog, even though about half of the characters are different if you compare the two strings letter-by-letter.
A promoter is like a word in this sequence, say "jumps"; a transcription factor will find places in the book with the word "jumps", and bind to that chunk of DNA. This will then influence transcription of the words that come after it.
In interpreting DNA sequences (or RNA, or protein) the solution to this general problem is called "sequence alignment", and sometimes it's fairly trivial and other times it's quite complex. There's a whole subfield of bioinformatics dedicated to these sorts of algorithms.

thanks a lot! Promoter seems to have some fixed semantical positions according to these -10 and -35 elements described in Wikipedia, isn't it?

@malocho Yes but remember these are all relative to something, not absolute positions.

ok, got it, thanks!


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Which co-transmitters are released first?
I understand that a single neuron can release different neurotransmitters depending on the frequency of its stimulation (see https://www.ncbi.nlm.nih.gov/books/NBK10818/). As the frequency of stimulation is increased, what is the order in which the neurotransmitters are released (i.e., which neurotransmitter is released at lower levels of stimulation and which are released at higher levels of stimulation)?

For a specific answer, you'd have to specify a specific neuron type. However, the source you link already discusses the general pattern, did you see that?

The source does say that smaller neurotransmitters are released first followed by neuropeptides; however I am looking for more specific information. Given the following list of neurotransmitters--glutamate, GABA, glycine, serotonin, histamine, dopamine, epinephrine, norepinephrine, endorphins, and acetylcholine--is there a specific order to which is released first based on stimulation frequency?

Those are all small molecules. No, it's not a list like that and it would be inappropriate to make one.

Why are we unable to make such a list?

Because that's not how it works. Read again the source you linked: it's not indicating that neurons release a dozen neurotransmitters in some order, it's saying that some neurons might release a couple different things, and that peptides tend to be released at higher intensities.

Maybe think of it this way: if someone says "people eat more than one thing for dinner, they often have their dessert after their entree", you wouldn't give a list of entrees and ask which entree is eaten before the other entrees.


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Why do the components of PCR mixture need to be added in a specific order?
I have recently been told that the components of a PCR mixture need to be added in a specific order: primers, dNTP, and finally polymerase. May I know why this is the case?

Welcome to the Biology Stack. Please take a [tour] and visit the [help] for more information on what we do here. Please also note the homework policy, which requires questions to contain evidence that the asker has attempted to answer the question for themselves. On that note; what do you know about those components and why might you add polymerase last (what does it do, and what could it do if you add it earlier?)?

you may be able to find your awnser here: https://biology.stackexchange.com/questions/79024/why-is-dna-polymerase-added-at-the-end-of-pcr-reaction

Polymerase last: One reson is that pipetting conditions are vastly differing by person, I.e. a lot of people don't keep the reactions on ice. When no hot-start polymerase is used, pipetting it in too early in a room temp. reaction mix might lead to unintended reactions.


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A DNA extraction protocol that is equipment-less for bacterial metagenomes?
I am going into the field soon to sample a very remote environment. For reasons that are unimportant here, I would like to extract bacterial DNA from these samples in the field.
I will have access to electricity, but no heavy equipment such as centrifuge. My goal is to extract DNA from these hypersaline liquids for long-read sequencing and subsequent metagenomic analysis with a focus on DNA methylation. My plan is to filter large volumes to have sufficient biomass onto a filter from which extraction will occur (think seawater type samples).
Any suggestions for an equipment-less DNA extraction kit? Vortexing is fine.

You'd be far far better off waiting until you can get them to a lab. Given the sensitivity of the technique and the unknown abundances and likelihood of getting samples, giving them the best extraction you can is the way to go. I realize this isn't always feasible and there are reasons not to do an extraction in the lab, but it is generally better. Fixing in ethanol on a filter would be fine to preserve until you can get it to a lab.
It would depend on the scale of preparation you want to do, exactly what you want to get out of it and the abundance of the bacteria in your samples. There are a number of para-magnetic bead based DNA (AKA SPRI beads) and RNA extraction products on the market. These are highly sensitive and quite quick to perform, but you do need the magnets and beads, both of which are quite expensive.
An example of this used for environmental bacteria is the following article. They did their extraction in the lab and used a centrifuge to concentrate samples, but it could easily be applied to the field:
Byrne RL, Cocker D, Alyayyoussi G, Mphasa M, Charles M, Mandula T, Williams CT, Rigby J, Hearn J, Feasey N, Adams ER, Edwards T. A novel, magnetic bead-based extraction method for the isolation of antimicrobial resistance genes with a case study in river water in Malawi. J Appl Microbiol. 2022 Nov;133(5):3191-3200. doi: 10.1111/jam.15755. Epub 2022 Aug 23. PMID: 35946113; PMCID: PMC9804433.

The reason to do it in the field is to avoid changes in the methylation pattern changing due to temperature shock when storing. One thing I may do is flash-freeze after storing in a buffer instead, but I did hope for a baseline to compare. Is ethanol the recommended storage buffer?

@donkey ethanol more or less fixes the DNA as it was at the time of addition. I don't know off the top of my head how you would proceed to with an extraction once in ethanol, but it should be fairly easy to do. EtOH fixed samples are one of the better sources for DNA from historical museum specimens and the like.


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Is there a quantitative report for cortical homunculus?
Almost all websites that I see for cortical homunculus only show the final picture with some qualitative descriptions such as "hands have more dexterity and occupy more motor cortex."
But is there a numerical table for their percentages?
Lips and tongue are big, but how big? 13%? 17%?
Is there a quantitative report for this?

I think you'd appreciate reading an 80-year update (Catani, 2017)) of the original paper (Penfield & Boldrey, 1937).
Four things come to mind (with commentary from Catani 2017 sprinkled throughout:

I would guess that certain inconsistency between individuals makes such a quantitative approach difficult.

Known overlap between body parts in any given region of the cortices makes such quantification tricky

From Catani, (2017):

Surprisingly, the picture that emerged from their work was a clear degree of functional overlap between stimulation fields rather than an orderly sequence of segregated areas as their homunculus suggests....

These maps indicate a high degree of overlay between different body parts, especially in the proximity of the central sulcus. Interestingly, the range of functional overlaps varies from expected—such as tongue and mouth, or arm and hand—to intriguing—such as mouth, arm and hand

How one determines the "regions" that each body part maps to can be done in various ways that would each create a different homunculus with parts therefore associated with slightly different region.

See Figures 2 and 4 in Catani, (2017) to see how redrawn homunculi vary in their relative proportions depending if they are proportioned based on stimulation areas, number of stimulations, or vertical length of surface maps for each body part.

The homunculus was never meant to represent quantitatively-discernable regions

From one of the original authors (Penfield) in a later publication:

such drawings may easily become confusing if too much significance is attributed to the shape and comparative size (Penfield and Rasmussen, 1950)

From Catani, (2017):

this little man, like many other figures that may naively populate our collective imagination, is just a metaphor for the complex neurological mechanisms that we strive to comprehend in their entirety

Note: I'm sure someone has tried to quantify as you've asked, so I encourage you keep looking. I would just guess that such efforts would best be found using search terms like "high field functional MRI" rather than "homunculi."

Citations:

 Marco Catani, A little man of some importance, Brain, Volume 140, Issue 11, November 2017, Pages 3055–3061, https://doi.org/10.1093/brain/awx270

 Penfield W , Boldrey E. 1937Somatic motor and sensory representation in the cerebral cortex of man as studied by electrical stimulation. Brain 60: 389–440.

 Penfield W , Rasmussen R. The cerebral cortex of man. New York, NY: The Macmillan Company; 1950.


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Is there a specific word for fertile hybrids?
The way "species" has always been described to me is that a species is different if the two animals cannot have fertile offspring, with the caveat that language is imprecise and sometimes different species can produce fertile hybrids. For example, "pizzly/grolar" bears, which are grizzly/polar bear hybrids produce fertile offspring. Another example is coywolves, which are wolf coyote hybrids. So, I was wondering if there is a specific name for fertile hybrids. The Wikipedia page on Hybrids doesn't specifically talk about fertile hybrids as a group. To be clear, to me, "fertile hybrids" is a sufficient descriptor. I just wanted to know if there was a more scientific term that is used in place of "fertile hybrids." My guess is that there is not, because I think I would have come across it by now, but I just wanted to be sure. Thanks.

"Admixed individual"? there are a variety of archaic and rather nasty words that mean more or less this, but as a society we have thankfully moved away from terms like "bastard"; "mongrel" is equally nasty when referring to people, but seems to still be standard for e.g. dogs.

The definition you're using for species there is called the "Biological Species Concept". It has a lot of problems.

In animals it is simpler, but in plants fertile hybrids are extremely common in certain families (e.g., Rosaceae) and even hybridogenous apomyctic lineages are often sexually fertile to a certain degree and give birth to new hybridogenous types that cause extremely complicated taxonomy in brambles, dandelions and similar.

Not that an exhaustive list is possible, but the hybridisation of neanderthals & homo sapiens is of particular interest, & undergone recent dynamic change in understanding. & the ape chromosome fusion that seems to have initiated the speciation of hominids, is an interesting example of a highly unlikely set of chance circumstances, leading to a significant biological change - a punctuation in equilibrium, rather than steady mutation.

I'm not aware of a single word term in use, "fertile hybrid" seems like a reasonable descriptor. Something like 4000 hits on Google Scholar so it appears it's definitely used, hybrid fertility matches about 3000. In cases where the hybridization is quite well known to be fertile, I'd expect people to drop "fertile" and just speak of hybrids, especially among plants (which may or may not be designated the same species; species are just labels and can be messy).
Another relevant term is introgression, which occurs when hybrids breed with one of the parent species and therefore has the ultimate effect of transferring genes from one species to another. Describing introgression as occurring also may clarify a bit what sort of hybrid fertility you're talking about, because it may be that hybrids are only fertile with one of the parent species, or either parent species but not another hybrid.

Another term related to introgression are hybrid swarms. Without introgression we can get hybrid speciation.

Genetically viable?

Genetic viability is the ability of the genes present to allow a cell, organism or population to survive and reproduce. The term is generally used to mean the chance or ability of a population to avoid the problems of inbreeding. Less commonly genetic viability can also be used in respect to a single cell or on an individual level.

authors: Vladimir F Героям слава


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Is proliferating stem cells dangerous on some aspects?
By searching on internet about replication of stem cells, I came across numerous articles speaking about how to activate stem cell proliferation, most articles searching "natural" means for that. This looks to me as some "magical words" for speaking of a good health.
My question is: what are the benefits of activating stem cells in our body, since:

Cicatrization mechanisms activate "when needed", when the body is underinjury
Activating stem cells could be a cause of tumors appearance (AFAIU)?

There are lots of different types of "stem cells" in the body, with many different roles, and varying degrees of "stem-ness". That article seems to be conflating iPSCs, which are highly pluripotent, with lineage stem cells like MSCs, with progenitor cells like the ones found in the crypts of the intestines that only differentiate into one or a few different cell types. It then combines this with a lot of hand-waving about good health practices in general. Basically the take-home should be that if you live a healthy lifestyle and eat well, your body will be taken care of. Duh.

Keep in mind the source of the article, too - they sell supplements just like the kinds recommended in the text. How surprising.

Thank you for your comments. I understand the "buy what I sell" side of the article, but my question is about proliferating stem cells in général. About the different type of stem cells, do some of them create cancers?

They can. And, in a way, all cancers have some stem-like qualities to them, as they proliferate continuously, given enough nutrients, blood supply, and protection from the immune system. Some "cancer drivers" are actually mutated or dysregulated genes that are active during stem cell proliferation and division. Stem cells can grow in a cancer-like manner, but they are typically regulated by surrounding tissue and the body as a whole, so they don't form tumors. It's only when that regulation goes awry that true cancers form.

So I understand that stem cells duplication can be activated by different elements entering the organism
But besides the nutrients, is there a need for "signalling" and "planning" of how and where stem cells will duplicate? Like an organ should not grow up in all directions

Yes, there's a tremendous amount of signaling and regulation going on. Stem cells don't just decide on their own to proliferate or differentiate, there's all sorts of inter-cellular signaling going on so each individual cell is acting in concert with its surrounding cells, as well as the needs of the tissue, organ, and body as a whole.

Would you have some information on this signalling and regulation. I think this is the path that answers the best my question

There's so much available online using Google or Google Scholar, and searching with terms like stem cell signaling or regulation of stem cell differentiation. It's a huge area of research, so you'll need to be more specific about what exactly you're looking for. This review might be a decent place to start.


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What is right below skin?
I was skinning a gopher so my cat can eat it (it was a pest and we didn't want to waste it). I thought its organs would fall out and make a mess, but that didn't happen. There was this sticky, transparent substance that surrounded its insides. What is this casing called? My dad said it was mucus but that isn't specific enough since there is mucus inside the stomach so I don't think they are the same.
I think this casing is found in all multicellular animals but I couldn't be sure.

Based on your reference to organs falling out and the overall description, I presume you're thinking of the abdominal cavity primarily, so there you'd be looking at the peritoneum or possibly the serous membranes of other organs (e.g., pleura, pericardium). These are membranous (in the general sense, not as a cell membrane) connective tissues covering the organs found in the abdomen and chest.
Other things you'll find underneath skin would include layers of fat, other connective tissues, muscle.
Here's a labeled image of a mouse dissection from Friedrich, L., Schuster, M., de Celis, M. F. R., Berger, I., Bornstein, S. R., & Steenblock, C. (2021). Isolation and in vitro cultivation of adrenal cells from mice. STAR protocols, 2(4), 100999.:

You might also look for dissections of fetal pigs or cats, which are commonly used in laboratory demonstrations for students (more often cats longer ago, more often fetal pigs these days).

Thank you for your great answer! I believe it is the peritoneum that I was observing.


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Is the Malaria vaccine the first vaccine against a Eukaryote?
RTS,S or Mosquirix was recently released to the public, offering the first Malaria vaccine. This struck me as particularly important because I don't know of any other vaccine that protects against organisms that aren't prokaryotes or viruses.
Is that accurate? Have there been any other vaccines developed for Eukaryotic organisms? I'm defining vaccine by the CDC definition: "A preparation that is used to stimulate the body’s immune response against diseases. Vaccines are usually administered through needle injections, but some can be administered by mouth or sprayed into the nose."
I'm interested in any developed vaccine that offered immunity regardless of relative effectiveness or side effects. Even if it wasn't released to the public.
Alternatively, if anyone has a definitive source indicating that the vaccine is the first of it's kind, that would also answer the question.

According to Wikipedia, in the entry for Giardiasis, there is a commercially available vaccine against Giardiasis that veterinarians can give to cats and dogs.  Giardia is a eukaryote.  https://en.wikipedia.org/wiki/Giardiasis


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How is melatonin production related to proteins produced by clock genes?
I am a high school student learning about feedback mechanisms. My teacher gave an example of how proteins produced by clock genes are related to melatonin production. However, I'm confused about the relationship between constant darkness, clock gene protein production, and melatonin production. My teacher said that constant darkness results in a drop in proteins produced by clock genes, but wouldn't melatonin production increase in constant darkness? Does this mean that the relationship between clock gene protein production and melatonin production is inverse? I would appreciate clarification on this topic.

I don't know much about this topic, in the absence of a real answer though, I'd suggest looking at a review paper on the topic: https://www.sciencedirect.com/science/article/pii/S0928425711000040?casa_token=VRcXQ1EiXEMAAAAA:1oQJp3oNyRn9cEIZqEhbU4RWHUoWDQDi3HSdYK5xsVixDhigc4gKMk_G8xmQdkf-jIE3WAHydus.


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Besides carbon dioxide and water vapor, what waste gases are removed through the human respiratory system?
Canadian Lung Association

remove the carbon dioxide and other waste gases that your body's doesn't need.

LibreTexts:

water vapor, carbon dioxide, and other waste gases move from inside the body into the outside air.

Cleveland Clinic:

cleans waste gases, such as carbon dioxide, from your blood.

Besides carbon dioxide and water vapor, what waste gases are removed through the human respiratory system?

It isn't just waste gases; any gas from the blood can diffuse into the lungs and be exhaled.

These sources are understandably couched in their language, but wikipedia is more certain:

All the metabolic wastes are excreted in a form of water solutes through the excretory organs (nephridia, Malpighian tubules, kidneys), with the exception of CO2, which is excreted together with the water vapor throughout the lungs. The elimination of these compounds enables the chemical homeostasis of the organism.

They go on to mention some other gases produced by other organisms such as denitrifying bacteria, but these are not related to the human respiratory system.
On the other hand, chemical analysis of breath apparently reveals a large number of volatile organic compounds (among other constituents), presumably related to metabolic activity:

In exhaled breath, more than 3500 different components have been found and the list is continually growing. The complex matrix of exhaled breath component is termed as molecular breath signature 2. The actual breath is a bulk matrix and contains mixtures of nitrogen, oxygen, carbon dioxide, inert gases, water vapor and a contain thousands of trace volatile organic compounds (VOCs) and inorganic molecules such as NO, NH3 or CO.

Moreover, a different distribution of such trace compounds appears to be diagnostic for some diseases, indicating that $CO_2$ is not the only waste business in town:

Human breath contains a myriad of biomarkers resulting from the blood by passive diffusion across the pulmonary alveolar membrane 2. Breath testing offers a novel approach to the disease diagnosis, evaluation of various common disorders, and assessment of exposure to VOCs [17].

I think that a good way of reading your quotes is as follows:
"Human respiratory waste gases include a lot of $CO_2$, which we understand pretty well why it's there, and a little bit of a lot of other compounds, which we don't understand very well."

Additionally to what Maximillian Press already answered, alcohol is also removed as vapour from the lungs. This fact is made use of in breath analyzers to measure alchohol concentration in the blood.


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Action Potential and Impulse Direction
My textbook describes generation of action potential due to an "induced increased membrane permeability to $Na$+ ions" and presents the ad hoc fact that electric current would flow from the depolarised site to other parts, through the axon till it reaches a junction.
This is mostly based on potential difference. However, my question is that when the impulse (or current) flows in the "conventional diretion (of neuron)", why isn't there a "backflow", i.e. can an action potential not flow back from a newly depolarised site to the originally depolarised site?
A possible intuitive assumption could be because of the differing potential differences, but I couldn't find a relevant explanation.

This is due to the refractory period at the end of each impulse. From here

The cell membrane cannot immediately produce a second AP. The period of time when the majority of voltage-gated Na+ channels are inactivated defines the ABSOLUTE REFRACTORY PERIOD, when no amount of depolarizing current can cause an action potential.

 Source: BYU
This refractory period is due to the gating mechanics of the voltage-gated sodium channels: From here

Refractory periods are caused by the inactivation gate of the Na+ channel. Once inactivated, the Na+ channel cannot respond to another stimulus until the gates are reset

Image
 Source: here
Because of the way impulse are propogated, this same principle explains why impulses are unidirectional under normal physiological circumstances. Again from BYU:

an action potential might have started near the cell soma and as it propagates down the axon towards the opposite end, the membrane potential behind the moving action potential has repolarized and returned to resting membrane potential. The axon ahead of the current depolarization has not yet depolarized and it is also at resting membrane potential. Where the action potential is occurring we find the membrane potential depolarized and the outside of the membrane at that spot is negatively charged relative to the inside of the membrane at that spot. As sodium rushes in, it will depolarize the next adjacent spot on the axon in the direction that the action potential is propagating. The reason that the action potential does not depolarize the section of axon membrane behind (or in the direction that the action potential just came from) is because that section of membrane is most likely in refractory periods and does not depolarize.

 Source: BYU
To demonstrate this, one could actually artificially trigger an action potential in the center of an axon (normally impossible) and observe it travel bidirectionally.


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Electrodes for electroporation of bacterial cells
Wikipedia says

"The process {electroporation} requires direct contact between the electrodes and the suspension."

However I've read the process is an effect of the field strength alone, and ideally no current passes at all, due to its heating and other unwanted effects. Why can there not then be a resistive layer between the electrodes and sample to stop any current flowing?

Hmmm, I'm not sure that this is the right site to answer this question - you might be better migrating to electrical engineering or  physics for a complete answer. I suspect that if it worked without direct current, then it would be done that way - perhaps you have a new idea and you can test it and potentially get a patent.


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Testing primer for misspriming in 770 Mb lepidopteran genome
I designed primer pairs for a lepidopteran genome (Cydia pomonella, codling moth, ~770 Mb, ~60% transposable elements, Reference Genome Paper). I have around 60 primer pairs that bind to a specific chromosome and now i would like to test for their specificity, meaning i would like to test whether or not the primers are mispriming somewhere else in the genome. I tried it using Geneious prime, but to test all primers for all chromosomes takes a lot of time. Then i tried the Primer-blast tool from NCBI, but unfortunately Cydia pomonella is not listed as an available target genome.
Do you have any experience on how to test the primer specificity on (large) genomes in a reasonable time? Another thought would be to blast each primer and see if it is aligning an known transposable element (if yes: discard the primer) and then ultimately try to optimize the PCR itself. Is there another way to test beforehand?

I added and then deleted an answer that says primer3. Unfortunately that does not appear to be true. I would suggest looking around for a blast-based toolkit that accepts bulk input for this purpose. I was not quickly able to find one but did find this helpful page with information about blast command line parameters that might be useful.

do you know biostars.org ?

Thanks for your suggestions, i will have a look in both :)


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Why does hypercalcemia cause muscle weakness, yet hyperkalemia causes muscle excitation?
The reasoning I've been given is that high extracellular $[K^+]$ increases the $E_v$ of potassium; therefore, membrane potential increases and the threshold for action potentials is more easily reached. Conversely, high extracellular $[Ca^{2+}]$ increases the accumulated positive charge outside the cell membrane and therefore increases the membrane potential.
However, like with $K^+$, wouldn't high ECF $[Ca^{2+}]$ also increase its $E_v$ and therefore membrane potential of the cell? Vice versa, high ECF $[K^+]$ should also increase membrane potential by accumulating charge.
Why are the effects different? A guess I had is that the relatively higher permeability of $K^+$ makes the effect on equilibrium potential larger than the effect of accumulating positive charge.

You're correct about your reasoning for potassium; high extracellular potassium concentration reduces the concentration gradient of potassium across the membrane, pushing the reversal potential for potassium towards neutral and therefore depolarizing cells due to resting potassium conductances.
For calcium it's quite different. Neurons and muscle cells are mostly impermeable to calcium at rest, and calcium is already high outside of cells relative to inside, so changing calcium concentration doesn't have any appreciable impact on resting potentials. From a pure ion-flow perspective, the primary change you'd expect in neurons is an increased action potential amplitude at the very peak: calcium reversal tends to be more positive than sodium reversal, so the very peak of the action potential is the part most influenced by calcium concentrations. This peak amplitude doesn't have much impact on all-or-nothing signaling, though.
You might also expect calcium concentrations to affect release probability of vesicles - that could increase neurotransmission.
However, that's not what's going on with muscle weakness. Instead, this is something special about calcium (well, divalent cations more generally) interacting with voltage gated sodium channels:

High Ca2+ levels (hypercalcemia) can block sodium movement through voltage-gated sodium channels, causing reduced depolarization and impaired action potential generation.

There's no way you can predict this from the principles of ion flow given by concentration gradients and voltages, and these sorts of things are why you have to do biological experiments with biology and not just computers: sometimes it doesn't work how you expect. The mechanism here is physical: calcium ions are big relative to sodium ions, but they have the same sign charge, so if possible, both would flow through a channel from the outside to the relatively negative inside. There's a place in the outer pore of voltage-gated sodium channels where calcium ions get stuck and just physically plug the hole. When a calcium ion is in the way, sodium can't flow (see Yamamoto et al 1984 and Santarelli et al 2007; the former looks at mechanism by altering voltage, the latter looks for specific residues on the channel that mediate calcium binding in the pore).
At typical low extracellular calcium levels, there aren't as many calcium ions around to block channels.

Santarelli, V. P., Eastwood, A. L., Dougherty, D. A., Ahern, C. A., & Horn, R. (2007). Calcium block of single sodium channels: role of a pore-lining aromatic residue. Biophysical journal, 93(7), 2341-2349.
Yamamoto, D., Yeh, J. Z., & Narahashi, T. (1984). Voltage-dependent calcium block of normal and tetramethrin-modified single sodium channels. Biophysical Journal, 45(1), 337-345.


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Why are mallards ornately green despite lack of sexual selection?
Mallards reproduce by group sex, with multiple males mating with a female against its will. This means that the common explanation of ornate birds evolving due to sexual selection isn’t applicable to them, so I’m curious why else they would evolve their green heads. Could it be a vestigial trait or are there any other explanations?

Do you have a reference for the claim that mallards reproduce without female mate choice?

there are a lot of studies of rape in mallards, that doesn't mean that the female mallard doesn't choose a mate and avoid the others, and you can also read about mallard pair behaviour, here's a broad overview: https://www.newscientist.com/article/dn11764-female-ducks-fight-back-against-raping-males/

The simple answer, as suggested in the comments, is that mallards are generally monogamous, with extra-pair copulations occurring but not canceling out the pairing, and with the note that some extrapair copulations are initiated by the female, e.g. female mate choice:

Once females had paired, it was observed that there was a trend for females to have displayed only at higher ranking males than their eventual partner (Wilcoxon signed ranks test, T+ = 30, p =.07). Of 10 females, eight displayed at more than one male. Out of 97 pairing displays by these eight females, only two by the same female were directed at a lower ranking male. Both these occasions were when the female's partner had displayed with another female and were directed at the next highest ranking male.

"Ranking" was essentially how quickly a male got into a pair, and it was strongly associated to breeding plumage (Table 1 of the paper). The sample size is a bit low, admittedly, but I'm sure the references of this paper have more to say about pairing behavior.
However you feel about "ranking" males, which I personally have mixed feelings about, this seems like a pretty textbook case of sexual selection.


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Population structure and SNP's in Linkage Disequilibrium
I am reading about population structure and how you could as an example use plink to analyze a set of SNPs for individuals in a vcf file to identify a given population structure.
I know that LD can be influenced by inbreeding, selection and genetic drift amongst others.
But for a given population, where the individuals who are not inbred, couldn't Linkage Disequilibrium also be used to identify population strucutre for the individuals present within a vcf file.?
So my question is, when would you use independently associated SNPs? when would you use SNPs in LD? or would you always simply prune those SNPs who are in LD?
Thanks for your time and help.

The answer hinges on a crucial distinction, which the difference between linkage and linkage disequilibrium.

linkage (physical linkage) is a measure of closeness on a chromosome between two loci. You can measure it in centiMorgans.
linkage disequilibrium (LD) is when genetic variants at two loci show a pattern of statistical non-independence. You can measure it using a correlation coefficient, or related statistics.

Linkage causes LD, but many other phenomena also cause LD, including (yes) common ancestry, selection, or even meiotic issues. There is no requirement that loci in LD be on the same chromosome.
To get at your question, yes, you could use LD to infer population structure or selection (examples linked), or other things.
Pruning SNPs in LD is used when you are making a strong assumption about the absence of LD. For example, using many SNPs in LD can lead to inflated estimates of heritability. This is because SNPs in LD are not independent observations, most obviously in the case of physical linkage. There is no point in observing 2 SNPs that are right next to each other in QTL mapping, for instance.
You would not want to prune SNPs in LD when you are doing any kind of haplotype-based inference, as just one example.
LD is a signal like any other, the question is whether you are interested in the non-independence of SNPs, or assuming the independence of SNPs.


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What is the mechanism behind antibiotic resistance and how can it be mitigated or prevented?
What causes antibiotic resistance, and how can we combat it? I am interested in the mechanisms behind antibiotic resistance and strategies to prevent it in bacteria.

We expect people to show at least some effort to solve a question by themselves. So, what have you found out? This is marked as homework which is used similar for low effort questions here.


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Confused about the transport of materials across cell membranes
I am very confused about how exactly substances are transported across cells. For example, if a cell is placed in a hypertonic solution, the cell loses water. If the cell is placed in a hypotonic solution, it gains water. This happens due to osmosis.
My confusion is, however, why don't any of the solutes within the cell move in or out of the cell instead of the water, to maintain an equal concentration inside and outside the cell? Why is it always the water in these cases that moves in and out of cells? Is it because the cell allows free movement of water, but it controls the movement of the solutes according to its needs using carrier or channel proteins? How exactly does the cell control what substance will move in and out during diffusion?

What does your source/textbook say about transport of materials across membranes? That's usually where these discussions begin, before getting into osmosis.

Really, basic osmosis is Chemistry, and in my experience always refers to semi-permeable membranes which, by definition allow water but not solutes across. As the most cursory research would make clear — research that we expect from posters to this site — what prevents polar solutes passing across a cell membrane is its non-polar lipid nature, making specific transporters necessary.

Before membranes and membrane transport, there's something called osmosis and diffusion to become familiar with. Because one of the roles of membrane transport of cells is to maintain osmotic pressure :)

A few short inputs:

The membrane is permeable for some molecules but not for others. Small and uncharged molecules can pass easily (such as H2O). Others like Sodium (Na+), Chloride (Cl-) etc. have a harder time doing that, due to electric charge (the membrane is hydrophobic, hence, energetically it doesn't really like to mix with something that is that hydrophilic). However, larger molecules can pass through the membrane, if they are very hydrophobic (think about different steroid hormones).
Furthermore, many ions, such as sodium, are actively transported in a particular direction. Water is usually not.
That is also, why when doing an osmosis experiment in a physics book you have a "semipermeable" membrane which only allows water to move across, but not ions. A cells membrane is basically "semipermeable".

I would suggest to read the chapters about transporters, ion channels etc. in a molecular biology book, such as "Molecular Biology of the Cell" from Alberts.

First you say 1) uncharged molecules can pass easily (such as H2O) but thereafter 2) the membrane is hydrophobic, hence, energetically it doesn't really like to mix with something that is that hydrophilic. These statements bite each other. Water is hydrophylic, since it likes itself :) Hence, it is lipophobic

Well, not necessarily. Water also doesn't mix very easily with membranes (water is still polar, membranes are largely not, at least on the inside). Otherwise they wouldn't be able to exist as stable entities. Think about oil (the membrane) and water. However, water, because it is fairly small and uncharged, can at least pass it regularly. That's why bacteria have things like aquaporins, where lots of water can get through the outer membrane (but not the inner membrane).

That's interesting, I'll read on it a bit :)

Felix, Cell or Berg & Stryer still would be quite up the ladder in my view. Start with AP chemistry and bio would be of some value.

By that comment do you agree that it is difficult for water to diffuse into the membrane and easier to pass through aquaporins? I am quite confused of what you finally have to say.

@Patrick Yes! :)

I would first like to define some terms first based on the permeability.
Impermeable: A membrane that does not allow any substance to pass through it is called an impermeable membrane. e.g. Cuticle layer
Permeable: A membrane that allows the free passage of substances through it is called a permeable membrane. e.g. Primary cell wall
Semi permeable: Semi permeable membranes allow the movement of most substances if they are small enough by osmosis or diffusion. It does not require any energy or in other words uses passive transport. e.g. Egg membrane
Selectively permeable: As the name suggests these membranes are more selective and the substance that can pass through are limited. Substances that cannot pass through by passive transport is transported by active transport through integral proteins embedded in the cell membrane.
Though the cell membrane acts semi-permeable to the small oxygen and carbon dioxide molecules it is best to call the cell membranes as selectively permeable membrane because of the degree of the control they have over on what to allow and not to. Try reading this page for the difference between semi permeable and selectively permeable.
You were right in saying that the cell membrane allows the free movement of water but controls the movement of other solute particles according to its needs. If the molecules are small enough and they are non-polar, they can easily diffuse inside. If they are polar , like water and glucose, it is difficult to push their way through the non-polar tails of the phospholipid bilayer. The channel proteins will aid in the movement of such substances through passive transport. The channel protein that allows the rapid flow of water through is called an aquaporin. If the substances need to move against the concentration gradient, from a lower concentration to a higher concentration, they use energy and pass through the proteins. This is active transport e.g. Sodium potassium pump.
And for the last question, diffusion is the net movement of substance from a region of higher concentration to a region of lower concentration. Note that this happens along the concentration gradient and does not need any energy. The cell cannot exactly "control" that movement. If the particle is small enough and the polarity is right, it can pass along the gradient. Movement of $CO_2$ out of the cell and movement of $O_2$ inside the cell is by diffusion.
Correct me if I went wrong somewhere.

"Water can pass through biological membranes via two pathways: simple diffusion through the lipid bilayer, or water-selective facilitated diffusion through aquaporins (AQPs)" Ibata et al., 2012


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What is the expected result when using Sanger Sequencing for Bisulfite analysis on an unmethylated CpG?
Hello fellow molecular biologists!
I'm currently starting out doing a lot of Bisulfite Sequencing and as COBRA is not sufficiently working on my sequence, I do Sanger Sequencing instead, as suggested by my PI.
The problem is I was told a single peak of "T" means the Cytosine is methylated, in a CpG context. However, thinking about it, I have trouble explaining how you would get to this conclusion.
My though was:
Imagine you have:
5' CpG 3'
3' GpC 5'
Now if both are unmethylated you get:
5' TpG 3'
3' GpT 5'
If you now do a PCR, they give rise to two types of DNA molecules (TG/AC) and (CA/GT).
If you perform Sanger Sequencing just with the forward primer, this would mean you get 50% "T" and 50% "C" at the original position.
In other words, the reverse strand (3'-GC-5') should always restore the "C" at the original position, when I perfom a PCR.
So who is wrong?
Should I expect 100% "T" or 50% "T" and "C" for a completely unmethylated CpG?
By the way, I asked ChatGPT. Initially he told me 100% "T" would be correct. As I explained my thought process, he agreed with me, but then cited imaginary papers with links that do not exist. :D
Thanks in advance!
Best regards, Felix

I would not go to ChatGPT for trusted scientific advice, it has a tendency to make stuff up, as you have discovered. I would suggest going back and interrogating further what "single peak of T" means. It is not easy to tell what it is supposed to mean from your question. Notably: does 50% T count as a peak? I would say so, if I was expecting C. If it's not the CpG context that's methylated but rather just that Cs are methylated, you would instead expect 2 peaks of 50%, right? Possibly misunderstanding.

"single peak of T" should mean that the sequencing result really just shows a clean "T", without any major peak for "C", "G" or "A" (hence the C being unmethylated).
To maybe elucidate that a little bit more: I'm really just aiming at analysing CpGs (not just Cs) and I try to conceptually get an understanding for what my result should be for a fully methylated CpG dyad, hemimethylated dyad (on one of the two strands) and fully unmethylated.
So the question is very straightforward. What would the Sanger Sequencing result look like, if the CpG dyad is fully methylated? And why?

Well, have you looked at the literature or wikipedia?

With all due respect, if your contribution is "read more" and have you looked on  Wikipedia, then I seriously question the motif behind you answering this question. It's really not that trivial if you think about it - and yes, I have read some papers about data interpretation of BS-Seq data and of course Wikipedia as well. So far I do not have found a comprehensive answer to what the expectation would look like (some just take the relative difference between C and T at the "C" position of a CpG) and to me the answer seems to be more complicated.

I am not trying to answer your question, or I would not have written in the comment field. I am trying to help you improve your question such that someone else can answer it (there are many people who are experts in this field but I'm not one of them). I'm sorry if this seems disrespectful. When someone feels prepared to answer your question, they will answer it in the "answer" field below. It is standard for people asking questions to directly cite the sources that they have already consulted and explain why they haven't answered the question; I am trying to help you to do that.

Thank you for the clarification. I wasn't aware of that.


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Recycling of nitrogen in hibernating mammals
Hibernating mammals are required to undergo profound changes in metabolism. In addition to the more studied requirement of providing energy, there are problems in relation to nitrogen metabolism because of the continued turnover of muscle protein and the need to dispose of the urea produced in the absence of urination.
In an abstract written over forty years ago Nelson states that to solve this problem urea is reconverted to amino acids:

“The urea that is formed is hydrolyzed and the nitrogen released is
combined with glycerol to form amino acids, which reenter protein
synthetic pathways.”

Is this correct and, if so, where does the process take place and what are the precise biochemical reactions involved?
N.B.
I am particularly interested in the hibernating bear.

some context https://www.nps.gov/katm/blogs/hibernation-in-bears.htm

Summary
The hibernating animal in which the recycling of nitrogen has been best studied is the ground squirrel. Recent studies in this species by Regan et al. (Science (2022) 375, 460–463) have provided strong experimental support to an idea proposed some time ago. This is that the ureases of gut microbiota hydrolyse urea to carbon dioxide and ammonia, the latter being incorporated into amino acids by these symbiotic bacteria. Some of the synthesized amino acids are taken up by the mammalian host and are used for its protein synthesis. It is reasonable to expect that intestinal microbiota may also play a role in other hibernators such as bears, but this remains to be established.
Proposals: Importance and Limitations
R. A. Nelson performed pioneering experiments in hibernating bears. He recognized that muscle protein did turnover, that this entailed disposal of nitrogen as urea, but that the blood concentration of urea was not raised (if it had been it would eventually have reached toxic concentrations) despite the fact that hibernating bears do not urinate. He realized that these two problems could be resolved if the nitrogen in the urea was somehow converted to nitrogen in amino acids, allowing synthesis of muscle protein to replace that which was degraded.

[Simplified diagram showing fate of nitrogen from amino acids resulting from protein breakdown in mammals]
In order to be incorporated into amino acids, nitrogen released from urea (as ammonia) needs a carbon skeleton to be integrated into, and Nelson proposed that this was supplied by glycerol produced from the lipolysis of triglycerides, which after phosphorylation can enter the pathway of glycolysis/gluconeogenesis in liver. Although the major rationale of this is gluconeogenesis to provide glucose for the brain, Nelson performed experiments with  14C-glycerol which showed that some radioactive label entered alanine, presumably by transamination of pyruvate produced by glycolysis of phosphoglycerate.
There are, in my opinion, two major limitations to this proposal. First, it would require a urease to be present in the liver to produce the ammonia for the transamination of pyruvate. There is no evidence of any mammalian urease, either experimentally or from the predictions of genomic sequences. Second, it would not explain how the degraded essential amino acids — amino acids the carbon skeleton of which mammals cannot synthesize — were replaced.
These difficulties were overcome in the proposal of Riedesel and Steffen for a role of gut microbes — rather than the animal itself — in recycling urea, although these authors studied small hibernating rodents, rather than bears. Their abstract specifically mentions:

…the potential for urea recycling by intestinal microbiota…

They had no experimental evidence that this occurred, but they argued for its feasibility in the context of contemporary knowledge at the time:

“Several monogastric mammalian species, including man, have been shown
to harbor microorganisms capable of urease activity (Long et al. Am.
J. Clin. Nutr. 31: 1367–1382, 1978).”

[Conversion of urea to ammonia and carbon dioxide by microbial ureases]
Evidence for role of gut symbiots in ground squirrels
The difficulty in performing experiments on either the microbiota or the animals themselves meant that it was over 40 years after the proposal of Riedesel and Steffen before Regan and associates published a paper with confirming evidence in the prestigious journal Science. They injected ground squirrels with 13C,15N-urea and determined its metabolic fate over the hibernation period by detecting the presence of these (stable, non-radioactive) isotopes using modern spectrographic methods. They also examined the abundance of urease gene sequences in ten individual bacterial taxa of the the metagenome. Their findings are conveniently summarized in the figure below, taken from their paper.

…and what happened to Goldilocks?
It remains to be established whether urea recycling through microbiota also occurs in bears, where hibernation has some different features. A 2021 review by Bertile
et al.  of protein sparing in hibernation includes a consideration of bears in an extensive and comprehensive coverage of this topic. There seems to be some reluctance to the idea of a major role for microbiota in urea cycling in bears, and the authors emphasize other factors that could contribute to protein sparing. It seems to me, as an outsider, that this reluctance will turn out to be unjustified, but, in the absence of experimental evidence, no conclusion is possible at present.

The ability for gut microbes to convert urea is not limited to hibernating animals. Cows  can do it too. Though only with ingested food. https://www.yara.com/industrial-nitrogen/animal-nutrition/animal-grade-urea/#:~:text=Urea%20can%20be%20used%20to,grazing%20feed%20quality%20is%20poor.

I finally managed to get the 1980 volume of Federation Proceedings with the articles by Nelson and by Riedesel and Steffen. I have made a final revision of my answer in the light of this (and also cut some fat). Because Federation Proceedings seems not to be available on line, and the effort of retrieving volumes from university library archives is considerable, I have temporarily posted scans of the two articles for any interested readers to check (linked names above).

@AsekuVena — Urease-producing bacteria are, in fact, found in the human microbiota (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4263730/) as well as in the stomach and urinogenital tract. The sort of questions of interest in relation to hibernating mammals  are whether the bacteria are relatively more abundant or have more active urease activity compared with non-hibernators (or in hibernators outside the hibernation period).


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Tiny insect identification in potted plants
Unfortunately, the new potted soil I've bought seems to be heavily infested with insects. Firstly, I have had a fight with fungus gnats. After using parasitic nematodes about 10 days ago, I no longer see them flying around, but there are still a lot of unwanted guests that I see moving around in the pot.
Can you tell what those could be? I live in Central Europe. The pests are quite small (ca. 1 mm in length) and are running quite quickly around the pot. They don't seem to be able to jump around. Unfortunately, due to their size and quite fast movement I was not able to take a good picture, but here are two specimens, marked with red arrows. Could those be the same or different species?

They might not be insects, but more basal hexapods like springtails.

Also, they are not necessarily pests. They have a pretty high change of being detritivores that break down waste, not really getting in anything's way and being more helpful than harmful.

These are a type of hexapod called springtails (Collembola).

 Common Soil springtails. Source: UMN Extension
Springtails vary in size, shape, and color, but most are < 6 mm long (as low as ~1 mm) and many tend to be dull white/grey/yellow in color.
Many species are omnivorous soil-dwellers preferring moist and organically-rich soils.

You will find them more frequently in over-watered plants.

For reference, I've had concurrent fungus gnat and springtail populations in my house plants before.
According to UMN Extension:

Springtails do not have wings and cannot fly. But they can jump up to several inches using a special forked structure under the abdomen

But these insects would very unlikely survive a jump out of your plant, nor do they want to do so -- they want to be near the moist soil. I would not worry about it. (though you could water less frequently to cause their population to drop if you're concerned -- but these animals are harmless and will often help with the breakdown of the soil or removal of some soil pests depending on species and ecology).
Sources:

Wikipedia

UMN Extension

FES Summaries

The variety in sizes in that photo is intriguing. Do you have any idea what that depends on? Is this a species that will continue growing for as long as it has food, perhaps, so larger ones are older? Is it some sort of sexual dimorphism? Something else?


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Are psilocybin/psilocyn the only psychoactive compounds in psychoactive mushrooms?
Psilocybe cubensis is the most common psychedelic mushroom, and its active ingredients are psilocin and psilocybin (which is converted to psilocin in the body).
There are other psychedelic mushrooms, such as psilocybe cyanescens, psilocybe mexicana, and amanita muscaria, as well as many others. Are there any other psychoactive compounds in mushrooms other than psilocybin and psilocin?
I found this page but wonder if it is exhaustive: https://en.wikipedia.org/wiki/List_of_psychoactive_plants,_fungi,_and_animals?wprov=sfti1

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

In particular, a Google search in the US for list of psychoactive compounds in mushrooms gives 8 different compounds, and there may be more.

Yes, there are multiple psychoactive compounds, including norpsilocin, baeocystin, norbaeocystin, and aeruginascin. Ergot and Fly-Argaric have different substances.
A lot of mushrooms contain ergot alkaloids to defend against nematodes and bacteria.
Alkaloids contain Nitrogen. They have biological effects like neurotransmission, circulation, hormonal, immuno-stimulant (lion's mane, chaga mushroom), immuno-depressant.
The psylocin group are very similar isomers:
Norpsilocin (4-HO-NMT) is tryptamine alkaloid recently discovered in 2017 in the psychedelic mushroom Psilocybe cubensis. It is hypothesized to be a dephosphorylated metabolite of baeocystin. Norpsilocin was found to be a full agonist of 5-HT2A receptor. It is also more potent than psilocin.
Baeocystin is a zwitterionic alkaloid and analog/derivative of psilocybin, and is reported to have similar strength and pharmacology.
Norbaeocystin is a N-demethylated derivative of baeocystin. phosphorylated derivative of 4-hydroxytryptamine. The latter is notable as a positional isomer of serotonin, which is 5-hydroxytryptamine.
Fly-argaric is also psychoactive via muscimol and ibotenic acid, a neurotoxin converting to muscimol after ingestion. Read the wiki page to find out the uses.
Lion's mane also changes neurotransmission..
To find current research, I suggest googling "neurotransmission funghi" and "funghi neurotoxin".
Flying is not the only measure of helicopters and planes, there's also landing, ground control, maintenance, cost, atmospheric events, efficiency and cargo events.

What does the last sentence add to your post?

@AliceD This friendly reminder disguised as an analogy might be referring to 'What goes up must come down' or 'No effect without side-effects'..


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Is there any risk for oranges to lose vitamin C
My understanding is that vitamin C easily undergoes oxidation. But for that to happen, the vitamin C has to be in contact with oxygen, e.g. with air. Therefore an orange doesn't start losing its vitamin C content by just because it's picked from a tree. It keeps that vitamin up to the moment we make juice out of it, when it starts losing it simply because it is dispersed in the liquid which is in contact with air.
That's what I know.
But somebody today told me otherwise, claiming that it's the plant that continuously supplies the orange with vitamin C.
This idea looks a bit silly to me, but I'm not a biologist, so I'm asking.
Incidentally, where in the orange is vitamin C contained? In each individual cell? I was once told that the oranges' cells (well, those that we like to eat and that actually make the juice) are those little drop-shaped things that are contained in the wedges (in a number that I'd say it's several hundreds?). Is that the case?

Isn't that what the covering is for?

@AsekuVena, I've also read that the peel itself contains more vitamin C then the rest

Maybe it is like the colony bacteria, who have their outer bits protect  the inner bacteria ?


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Identification of these birds
We recently put up a bird house and put a camera in it. We appear to have two new neighbours, but what is the species?
We live in the south-western part of Norway.

This is very likely the great tit (Parvus major).

Photo by Walter Baxter.

this is probably the most common bird in norway,if i step outside my house in daylight i will see one in less than 5 min.


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Leaf pictures: Which disease?
I had several plants that with same symptoms, which all eventually died within some weeks: Formation of blisters along stem (no picture) and leaf veins, that seem to pop up (assumption) and make everything around sticky. The disease started with citrus plants (diverse limes) that I bought.
I thought it must be a some microorganism, but strangely close-up pictures resemble some flea-like morphology of the blisters, which makes me so curious that I ask this question. The plant leafs are Kaffir limes, approximately 6 cm long.
Also, would you have any idea how to save my plants?

I forgot to say, you can scrub them off with a toothbrush, but that won't kill the eggs. Needs to be repeated several times. Good luck!

Great, I will try that!

It looks like a scale insect to me, similar to Citricola scale but lighter in color. It might be a Soft Brown Scale, but they usually appear multiple generations at a time, so you'd see all sizes from tiny to full grown, whereas citricola scale usually appears as a single generation (all approximately the same size.) Either way, they suck the life out of plant leaves and will reduce their vigor and setting of fruit, while secreting a sweet liquid that promotes fungal growth.
When I see a scale insect, it gets scraped off the plant with my fingernail or a knife (and smooshed), and the leaf gets cleaned. If the leaf has been injured, I either get rid of it or rub a tiny bit of a mixture of beeswax and olive oil on the spot. Clearly this won't work for you. As I don't use any insecticides (unless you count my fingernails, etc.), I can't give you any advice about control, but it should be easy to search online.

Photograph from the United States National Collection of Scale Insects Photographs

It is only necessary to scrape them off with a nail ; they will not reattach.

That's true, but I don't like plant pests... If insects in my garden are unsightly but basically harmless, I leave them alone. If they are harmful, they are no more.