text:
Converting from RU/ML to AEU/ML
I'd like to know whether it is possible to convert from RU/ml to AEU/ml.
I work in the ELISA department in our laboratory. We need to validate some kits by comparing results between our lab and another lab. They reported their values using the AEU/ml unit whilst ours are in RU/ml.
Is it possible to convert between AEU/ml and RU/ml?
RU: Relative Unit   AEU: Arbitrary Elisa Unit. The plates are read on a Biotek microplate absorbance reader via UV-VIS detection at a wavelength of 450.
Thanks in advance!

For those that aren't familiar with the terms, can you please [edit] your post and define RU and AEU? Also, what format is the ELISA readout - colorimetric, luminescent, fluorescent, or MSD?

RU: Relative Unit   AEU: Arbitrary Elisa Unit. The plates are read on a Biotek microplate absorbance reader via UV-VIS detection at a wavelength of 450

How are these units calculated? If both labs run the same set of standards to plot a linear standard curve, you should be able to make a simple mathematical calculation to convert from one to the other.

For example, if a 1 μg/ml standard gives you 1000 RU and 5000 AEU, and a 5 μg/ml standard gives 3000 RU and 10,000 AEU, you can use curve-fitting to get the formulas for each line, then figure out a translation function. Alternatively, you can use their formula for determining AEU from the raw OD450 and back-calculate your own values.


text:
Can I safely handle this caterpillar?
I just found this caterpillar in my garden. I’m about to mow the grass for the first time. Can I safely handle it? What type of caterpillar is it?
For reference, I’m in Leeds, UK. Here are some pictures:

It’s about 5cm long and 1cm wide. Thanks

After a bit of Googling I think I found it. It’s a pale tussock moth caterpillar. https://butterfly-conservation.org/moths/pale-tussock
It says it irritates the skin and can cause a nasty rash so I’m staying away for now.
I might risk moving it with a trowel and small tub though.

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sort: votes


text:
How is it thought that phosphine is synthesized by living organisms on Earth?
The recent (Sept. 2020) report of “Phosphine gas in the cloud decks of Venus” states that phosphine (PH3) is only known to occur on Earth due to anaerobic life. Quoting from a report in the New York Times:

But scientists have yet to explain how Earth microbes make it.
“There’s not a lot of understanding of where it’s coming from, how it forms, things like that,” said Matthew Pasek, a geoscientist at the University of South Florida in Tampa. “We’ve seen it associated with where microbes are at, but we have not seen a microbe do it, which is a subtle difference, but an important one.”

What are the current hypotheses about how phosphine is formed?

I haven't had a chance to read the full Nature Astronomy paper, but I would assume that the authors cover at least some of this in there.

@MattDMo — Not really. One of the co-authors of the paper is also an co-author of the paper I quote in my own answer, and her work is referenced. But the problem would seem to be that the conditions in which phosphine appears to be produced biologically on Earth, are very different from those in Venetian clouds.

The number of researches of venusian phosphine will promptly go up to the thousands, measuring and detecting all the other biological signatures which can exist on venus astronomically and in the lab, and there will be some high-profile critics of the study. A lot more evidence will be coming in soon, for the moment it's a bit murky.

I have made some presentational changes to your question, given that what was "today" is now yesterday and tomorrow... I also thought it fairest to describe the Nature Astronomy paper using its exact tile, gave the formula of phosphine, and added the astrobiology tag. Hope that's OK.

The background to phosphine production on Earth can be found in a review entitled “Natural Products Containing ‘Rare’ Organophosphorus Functional Groups” by Petkowski et al. in Molecules 24, 866 (2019). The four authors are also co-authors of the Nature Astronomy paper. They state (my emphasis):

The detailed biosynthetic pathway for microbial phosphine production
is currently unknown. For detailed discussion of the biological
production in the environment, its biochemistry, and atmospheric
chemistry see three recent papers by Bains, Sousa-Silva and colleagues
[482,494,495].

These three papers are from the authors, one of which I followed up:

Bains,W.; Petkowski,J.J.; Sousa-Silva,C.; Seager,S. New environmental model for thermodynamic ecology of biological phosphine production. Sci. Total Environ. 2019, 658, 521–536.

The abstract to this includes (my emphasis):

In this paper we show through thermodynamic calculations that, in
specific environments, the combined action of phosphate reducing and
phosphite disproportionating bacteria can produce phosphine.
Phosphate-reducing bacteria can capture energy from the reduction of
phosphate to phosphite through coupling phosphate reduction to NADH
oxidation. Our hypothesis describes how the phosphate chemistry in an
environmental niche is coupled to phosphite generation in ground
water, which in turn is coupled to the phosphine production in water
and atmosphere, driven by a specific microbial ecology.

The paper itself is not of the ‘author-pays’ type, so you may need institutional access to read it. There is a graphical summary provided, however, which summarizes the hypothesis:

The paper consists of detailed thermodynamic arguments for the scheme suggested at the particular temperature, pH and anaerobic environment of marshes and swamps. Under these conditions, the authors postulate that the purpose of posphine production is to gain energy†. The analogy would be with the production of NADH as in anaerobic glycolysis to gain energy, but needing to be reoxidized to NAD+ to allow this to continue. The reduction of phosphate to do this would be analogous to the reduction of pyruvate to lactate or to ethanol. Like ethanol, phosphine would be a by-product of no value to the organism.
However the possible role envisaged for phosphine production in Venusian clouds is different. In the Supplementary Information for the Nature Astrobiology paper, there is the following:

Initial modelling based on terrestrial biochemistry suggests that biochemical reduction of phosphate to phosphine is thermodynamically feasible under Venus cloud conditions. Biological phosphine production on Venus is likely to be energy requiring. However, life can make substantial energy investment into compounds that provide important biological functionality. There are many potential useful biological functions including signaling, defense, or metal capture for which phosphine has useful properties, so endergonic biosynthesis cannot be ruled out.

The suggestion here is that phosphine is a useful product, synthesized at an energetic cost.
The only biochemical connection between the two would be that if, as appears likely, life on Earth can produce phosphine (by biochemical pathways that remain to be discovered), then these same biochemical processes would be candidates for phosphine production by life on Venus if the authors are correct in arguing that (at least known) non-biological candidates have been excluded. The question does not ask for opinions on the latter, nor would I presume to present those that I hold.

† The thermodynamic approach involves calculation of Gibbs Free Energy changes (ΔG) for reactions. Often on this site discussing standard biochemistry we (or at least I) talk in terms of standard free energies — ΔG˚ (or ΔG˚′ for normal cellular conditions). However the actual value of ΔG for a reaction is influenced by temperature and the concentration of reactants (which will include hydrogen ions), so that the ΔG calculated for terrestrial marshes and the like is likely to differ from that in Venusian clouds.

The paper also appears to be on arXiv  https://arxiv.org/abs/2009.06593

@usernumber — That is a preprint of the Nature Astronomy paper, the final version of which is freely available, I believe. However, clearly some people have known about it for a while.

It looks like a good read of Bains's related work would be of interest to the OP.  Trivalent Phosphorus and Phosphines as Components of Biochemistry in Anoxic Environments is another that looks worthwhile (though I come to this from the physics side).  According to the Nature Astronomy paper (Greaves et al) Bains has another paper on the way, but that's more on the Venusian side.

I guess the reasonable follow-on question would be whether the process described there could feasibly operate in the sulfuric clouds of Venus.

@T.E.D. The atmosphere in Venus is mostly carbon dioxide. Only a trace amount of sulfur is found. Also, hydrogen was theorized  to have present in relatively short supply in the Venusian atmosphere but most of them is lost to space with the remainder(trace)  being bound up in sulfuric acid and hydrogen sulfide. Also, the Vesuvian clouds composing of sulfuric acid are formed in the upper atmosphere. Even if it rains, it evaporates around 25 km above the surface and thus not affecting the microbes present in the ground. But research is still going about the feasibility of this cycle on Venus.

@T.E.D. I'm sure that's discussed in Bains's new 103-page preprint

Detection and role of phoshine in phosphorus cycle was first discussed in 19881. They examined phosphorus cycle in open-air sewage treatment plants where they discovered a gas releasing from sediments of 1-2 meter deep water which was found to be phosphine. They calculated that 5 g of phosphine was released from 2000 m3 of sewage. They also further proposed that:

Under laboratory conditions, it was also demonstrated that phosphine
is released by bacterial reduction from a medium containing
inorganic phosphorus. The phosphorus content of the medium decreases
by nearly one half.

This bacterial reduction of phosphine was further explained in a 2000 paper2(Also see ref. 3):

A microbial basis for bioreductive generation of phosphine is
proposed, which could account at least in part for the presence of
this toxic gas in natural anaerobic environments and in sewage and
landfill gases. Phosphine generation under anaerobic growth conditions
was dependent upon both the culture inoculum source (animal faeces)
and enrichment culture conditions. Phosphine was detected in headspace
gases from mixed cultures under conditions promoting fermentative
growth of mixed acid and butyric acid bacteria, either in the presence
or absence of methane generation. Monoseptic cultures of certain mixed
acid fermentors (Escherichia coli, Salmonella gallinarum, and
Salmonella arizonae) and solvent fermentors (Clostridium sporogenes,
Clostridium acetobutyricum and Clostridium cochliarium) also generated
phosphine. Generation of phosphine by these
bacteria could explain the apparent correlation between methanogenesis and the formation of phosphine in nature.

But this phosphine reduction was found to be thermodynamically unfavorable and hence a proper biochemical reduction pathway has not been identified4:

Thermodynamic considerations indicate that it is very improbable that
the reduction of phosphate to phosphine is endergonic. Therefore the
generation of phosphine cannot be compared with sulphidogenesis and
methanogenesis. There seems to be a link between the existence of
highly reactive gaseous phosphorus compounds and increased levels of
metal corrosion. The reactive compounds could be formed by
micro-organisms or they are liberated from phosphorus-containing
impurities in the iron by the action of bacterial metabolites. The
biochemical pathways responsible for the production of gaseous
phosphorus compounds have not been characterized yet.

But then in a 2014 paper, a possible redox reduction method has been proposed5:

No other common reducing agent can produce phosphine at the
concentration at which it is observed in nature, as reduction from
phosphate is energetically unfeasible unless phosphite or
hypophosphite are present in the environment (important members in
phosphorus cycle). Phosphite and hypophosphite generate phosphine and
phosphate from disproportionation reactions:
$$\ce{4H2PO3^− + H+ -> PH3 + 3H2PO4−}$$
$$\ce{2H2PO2− + H+ -> PH3 + H2PO4−}$$
Phosphine production is primarily dependent on the concentration of
phosphite and hypophosphite, but is also dependent on pH, temperature,
and total dissolved P concentration. If the majority of the reduced P
occurs as hypophosphite, then more PH3 should be expected
than if the reduced P occurs as phosphite.

Conclusion: Phosphine should be/is considered to be an integral member in phosphorus biochemical cycle as it is found to be formed from the reduction of phosphites/hypophophosphites (important members in PBC). About 10% of the phosphorus produced in the atmosphere from PBC is PH3. Direct production of phosphine gas occurs in some specialized, local conditions like deep-marine environment where PH3 concentration was found to be 0.01 ng/m3 - 100 ng/m3.
PBC is itself an important process for sustaining life on Earth. It synthesize life-sustaining molecules important for the biosphere. Since, it is found in Venus, we can hypothesize anaerobic life on Venus although it hasn't been confirmed yet. In future, we might see life on Venus.
References

Dévai, I., Felföldy, L., Wittner, I. et al. Detection of phosphine: new aspects of the phosphorus cycle in the hydrosphere. Nature 333, 343–345 (1988). https://doi.org/10.1038/333343a0
Jenkins, R & Morris, T & Craig, P & Ritchie, A.W & Ostah, N. (2000). Phosphine generation by mixed- and monoseptic-cultures of anaerobic bacteria. The Science of the total environment. 250. 73-81. 10.1016/S0048-9697(00)00368-5.
Liu Z, Jia S, Wang B, Zhang T, Liu S. Preliminary investigation on the role of microorganisms in the production of phosphine. J Environ Sci (China). 2008 ;20(7):885-890. doi:10.1016/s1001-0742(08)62142-7
Biological formation of volatile phosphorus compounds
Joris Roels, Willy Verstraete, Bioresource Technology, Volume 79, Issue 3, September 2001, Pages 243-250, DOI: 10.1016/S0960-8524(01)00032-3
Phosphorus redox biogeochemistry, Matthew A. Pasek, Jacqueline M. Sampson, Zachary Atlas, Proceedings of the National Academy of Sciences, Oct 2014, 111 (43) 15468-15473; DOI: 10.1073/pnas.1408134111

"Conclusion: Phosphorus biochemical cycle is an important cycle for sustaining life on Earth." I don't wish to be critical of another answer, but I cannot see how this statement can be concluded from the (excellently presented) information you present. You make no mention of a cycle or explain the fate of the phosphine. Even if it is reoxidized to phosphate, you do not state how much it contributes to overall phosphate availability. Phosphorus is a necessary component of living things, but I doubt that it depends on a phosphate/phosphine cycle.

@David Thank you for the feedback. I tweaked my answer a little bit.

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text:
How do organophosphates affect kidney function?
Many organophosphates, besides inhibiting acetylcholinesterase, can also permanently inhibit the enzyme neuropathy target esterase, leading to nerve damage. NTE also happens to be found in the kidneys, and is involved in osmolyte production. Have organophosphates been known to affect kidney function through the inhibition of NTE in the kidneys? If so, how?
Source:
Gallazzini, M., & Burg, M. B. (2009). What’s New About Osmotic Regulation of Glycerophosphocholine. Physiology, 24(4), 245–249. doi:10.1152/physiol.00009.2009

One article suggests that NTEs in kidneys are important for regulating NaCl concentrations, whereby if increasing concentrations of NaCl are sensed in inner medullary collecting duct cells transcription of the building blocks of NTEs are increased to decrease this NaCl. If NTEs are inhibited due to being irreversibly bonded with moieties of organophosphates at their active sites then this would mean that the kidneys would lose their mechanism for controlling how much salt is excreted from the body.
Gallazzini, M., Ferraris, J. D., Kunin, M., Morris, R. G., & Burg, M. B. (2006). Neuropathy target esterase catalyzes osmoprotective renal synthesis of glycerophosphocholine in response to high NaCl. Proceedings of the National Academy of Sciences, 103(41), 15260 LP – 15265. https://doi.org/10.1073/pnas.0607133103
This loss of chloride and sodium, I posit, would then have a knock-on effect on the concentration gradients maintained in the kidney as necessary for effective absorption and excretion of other ions. My guess is that hyponatraemia would be one of the direct results of the presence of organophosphates in the kidneys.


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Does electrotonic spread/conduction occur in saltatory conduction?
Even as textbooks, and almost all web pages I've seen so far, explain electrotonic spread/conduction as the passive current flow along an axon, they do so with continuous conduction only. Apart from myelin sheaths which enwrap axons leaving only the Nodes of Ranvier exposed, and of course, the energy requirement and speed of conduction differences, I can't see how else continuous conduction differs from saltatory.
My question then is why electrotonic spread is never mentioned in saltatory conduction.

Generally textbooks take the following pedagogical flow in basic neurophysiology:
Ions flow, so voltage changes propagate
This is the "electrotonic part". The key concept is that if you add some ions or change the voltage of one part of a neuron, adjacent areas will also change in voltage as current flows 'passively'. The further away you go, the longer it takes the signal to arrive and the smaller it will be as the charge spreads out.
A more advanced course might also talk about the sources of those charges, like sensory receptors or neurotransmitter action, and might talk about the ways that polarizing pulses integrate over space and time. Or these may be saved for later.
(side note: in reality, neurons aren't all that passive, there are lots of conductance changes occurring even in this supposedly "electrotonic" scheme, but the electrotonic equations tend to work pretty well, and in a simplified experimental system they are sufficient. Biology is almost always too complex to try to include everything at once)
Action potentials
The key concepts here are that if the voltage changes enough, it stops being possible to think about just the passive flow, you now have to think closely about voltage-gated channels that create a positive feedback loop response to voltage. Above threshold, voltage-gated channels cause sufficient depolarization that adjacent areas of the membrane are also depolarized beyond threshold, and we call this propagating signal an action potential.
At this point, you are supposed to remember and understand that what is driving this active response is still a somewhat "passive" flow of charge that you understood from the "electrotonic" part of the course. That part is the physics and is always present, you can't get rid of it. However, you're in a new scheme where you can't use the electrotonic equations to understand what happens anymore.
Saltatory conduction
Myelination and saltatory conduction comes next. In this section, you're supposed to be thinking about the way action potentials spread, but to add one extra little wrinkle. What if, instead of transmitting piecemeal to the next adjacent segment of membrane, axons were more insulated? In this scenario, the flow of charges will extend much further. You should still be applying the concepts you learned in the "electrotonic" part, though: if you add some ions/change the voltage of one part of the neuron, adjacent areas will also change in voltage as current flows. The further away you go, the longer it takes the signal to arrive and the smaller it will be as the charge spreads out.
Therefore, even though insulation lets the signal travel further, it still decreases in amplitude over long distance, and you need to "boost" the signal again. That's where nodes of Ranvier come in.
Back to your specific question...
"Does electrotonic spread/conduction occur in saltatory conduction?" - No, but not because the "physics" part is different: saltatory conduction is necessarily active (involves voltage-gated channels), not electrotonic, even though all the electrotonic principles still apply.
The "electrotonic" part of the lesson contains important concepts that you are supposed to remember and carry through the other sections, even if it's not discussed explicitly. I think making that active/passive distinction is possibly a bit misleading, but the concepts you are supposed to grab from the electrotonic section in terms of the physics of how charge/voltage moves around in a neuron applies to everything.
Additionally, you should gather that the nodes of Ranvier are spaced in order to conduct action potentials. These are big voltage changes. Smaller voltage changes that are subthreshold will of course also travel down the axon (this is the physics part - nothing stops physics!), but if they aren't strong enough to open voltage gated channels at the next node of Ranvier then the voltage change isn't of any consequence and just decays with distance. If it was strong enough, then by definition it is superthreshold rather than subthreshold, and we are talking about an action potential.

All the content in this answer is material like you would find in a basic undergraduate neuroscience textbook. The ones I usually recommend are Purves or Kandel.

Ok. Since the passive current actually flows, why don't we say electrotonic potential is a propagated response? Because of its reduction in amplitude as it moves?

@Chemo-Mike Yes, it's "propagated" locally in the cell (so you will observe spatial summation of potentials at different nearby dendrites), but not propagated down the axon so cannot typically influence other cells.


text:
Low-tech or low-cost technique for quantitative estimation in enzymology
If an accurate measurement of enzymologic quantities is needed, then following established methods in the field is necessary.
However, it is sometime of great usefulness to ballpark a value before committing to taking the necessary time for protein purification, or buying the necessary equipment/reagents.
For such purpose a little "hack" can go a long way. This often involve using an available equipment
to substitute for another (e.g. maybe I have a FACS readily availably, however no HPLC).
I am seeking examples of "unconventional" use of lab technique that
can be used to determine enzymologic quantities ($K_d$, $V_{max}$, $K_i$ ...) as a first estimate -- whether you have partaked in such heresies, or have merely seen them used, possibly even in a non-formal/DIY environment.

With bacteria, we often use selective or differential media to determine presence or absence of certain enzymatic reactions. Would that sort of think be useful? Probably wouldn't be able to estimate an enzyme kinetics that way though.

If there is a way to:

Make the replication of a common culture organism (e.g. E. coli) dependent
upon the inhibitor or substrate of interest, possibly with a restrictive media.
Express the enzyme of interest in a relatively controlled manner in such organism (e.g. well caracterized promoter in plasmid with well characterized copy number),

Then you can get good mileage out of some serial dilutions and a OD600 meter. Even better with a plate reader.
Exact protocol will depend on the quantity under consideration, but mostly will amount to substituting around in the enzyme kinetics equations until the quantity of interest is a function of the concentration, and devise a scheme to cancel out the other unknown quantities (often substrate concentration ramp + starting OD ramp + curve fitting)


text:
Biosafety Level 1 (BSL-1) surrogate viruses that show greatest similarity to SARS-CoV-2
I would like to know if there are any viruses that show high similarity to SARS-CoV-2 (particularly in terms of structure) that are very safe to use (i.e., classified as BSL-1).
For example, an avian coronavirus would be good to use but it is BSL-2. Ideally, I would need BSL-1.
Ideally if there were any corona type viruses that were BSL-1 or those which have distinguishing features with proteins emanating from an outer lipid membrane similar to SARS-CoV-2 .
I am particularly interested in finding a virus with similarity to the protruding S1 spike in SARS-CoV-2 (see image).

Can you be more specific about 'structure' and 'similarity'. Do you mean similarity in RNA sequence, protein sequence, function, pathogenicity etc?

Good question! Thanks for your comment. I mean in terms of its most outer appearance/structure. e.g., anything with a similar protruding protein stricture on its outer membrane.

I added an image too to illustrate that I am interested mainly in any similar viruses that have similar outer protein structures.

To be further specific. I'm thinking in terms of how it would interact with a (generic) surface. So any virus that is classified as BSL-1 that is similarly covered in protruding protein and/or would interact with a given surface (be that a window, door or even a host cell) in a similar manner.

What you're looking for is a suitable surrogate. For H1N1 the surrogate used was MS2 coliphage. I recommend going onto https://viralzone.expasy.org/294 and looking at the coronaviridae family. Then find viruses in this family and go onto the atcc website and see what classification BSL a certain strain of the virus is (be careful not to confuse it with genomic RNA from the virus). Adenoviruses with spike cloned onto them (what astra zeneca is doing) could also be an option, but last I checked this was only BSL2. Maybe Orthomyxoviridae (family of influenza) might have some genetically modified.

Thanks for this info! Very useful. I am not a biologist by training. Navigating this space effectively is a little difficult to me as much of the terminology is alien to me. I'm suprised a suitable surrogate has not already been identified. In my case, I'm after a safe and suitable surrogate which is representative of the coronaviridae family in general based on its outer protein conformation. Any other suggestions?

Some specific examples would be awesome if anyone can provide some? even if you are not very sure. it would be a big help. thanks


text:
Why do coronavirus cases graphs have a sinusoidal like shape?
Some screenshots from a canadian website:

See this sinusoidal shape? Why is it there? Shouldn't it be a single curve?
My main guess is when cases are counted: is it possible that they are counted something like every monday or so? I can't believe the virus progression really has sinusoidal-shaped curve.
It is not an error in the website, since other sources seem to show the same thing: worldometers, nbc news, and many others

I think you mean SINE, not SINUS.  They're different words, with different origins. https://en.wiktionary.org/wiki/sine#Etymology vs https://en.wiktionary.org/wiki/sinus#Etymology

@jamesqf The page you liked says that sine is a "Doublet of sinus". Hence, they have the same origin. And since the OP has a non-English name, they probably speak on of the many languages where the function is indeed still called "sinus". For example, https://en.wiktionary.org/wiki/sinus#Noun_7

I did mean sine, thanks for the info. The sine function is labeled "sinus" in french.

It's a weekly cycle due to reporting disruptions over the weekend.
Use a 7-day moving average to get a better picture. Holidays and such can still be disruptive but the 7-day average solves most of it.

That's what happened in the UK. Most hospitals didn't report on Saturday / Sunday / Bank holidays, a small number did. The results published were based on the reports of the day before. So Saturday result = normal, Sunday result = low, Monday results = low (because little got reported on Sunday), Tuesday results = very high (most of Saturday / Sunday got reported on Monday), Wednesday results = slightly high (some hospitals didn't manage to report everything on Monday).

And then we had newspapers that reported every weekend how we are beating the virus because the numbers dropped, and every Tuesday how we were struck by total disaster because the numbers went up.

authors: Vladimir F Героям слава


text:
Transcription of two different factors from the same transcription factor - seeking a relation between concentrations
Let's assume that:
Factor $X$ enters nucleus and results in the transcription of two different factors, $A$, and  $B$.
$X$ $\to$ $A$
$X$ $\to$ $B$
Can it be expressed as
$[A]=\alpha [X]$ or  $[A]=\frac{\theta (\alpha [X])^n}{1+(\alpha [X])^n}$ and
$[B]=\beta [X]$ or  $[B]=\frac{\theta (\beta [X])^n}{1+(\beta [X])^n}$
where $\theta$ is the Hill coefficient, such that concentrations of A and B have a relation between?
Note: I don't have an education on molecular biology, or biology - terminology might be wrong.

This question definitely needs more details and clarity, especially regarding the Hill coefficient, what $\alpha$, $\beta$, and $n$ are, and what specifically your question is. However, from what I do understand, from a biological perspective the answer is "not necessarily". It is entirely possible that one or both of the factors $A$ or $B$ has an inhibitory effect on the activity of $X$, causing it to be produced more slowly (and eventually turned off) as its concentration increases. This is actually a very common occurrence, and doesn't seem to be accounted for in your equations.

@MattDMo thank you for writing a comment, X, A and B are known factors, X is the nucleus triggering factor of a long molecular cascade. A and B effects the upper factors on the cascade and after $\delta t$ they effect X too but I am focused on the immediate time step between X and transcripted factors. $\alpha$, $\beta$, and $n$ are hypothetical. I hope it clarified things a bit.


text:
Why are some organisms able to regenerate?
Why can sponges, cnidarian polyps and planaria regenerate if broken up, but other animals e.g. humans and phylum chordata cannot?

All organisms, including humans, have the ability to regenerate something in the body. But the process is much more developed in lower organisms such as plants, protists -- unicellular organisms such as bacteria, algae, and fungi  and many invertebrate animals such as earthworms and starfish. These organisms can grow new heads, tails, and other body parts when injured.
Scientists don't know why mammals don't have the same ability to grow new limbs. But they think it is because mammals have more complex biological structures; limb regeneration would require sophisticated controls to ensure that limbs and organs don't grow out of control. Humans, for example, are already equipped with safety mechanisms to ensure that individual cells don't grow uncontrollably. But these mechanisms wear down as a person ages and cancer is often the result.
Nevertheless, mammals do regenerate skin, muscle, and blood. Scientists are just beginning to learn about other types of cells, such as those in the brain and blood, that also regenerate. Further study of the phenomenon might lead to a way of growing replacement organs and limbs outside the body.
Not all organisms regenerate in the same way. In plants and organisms like hydra and jellyfish, missing parts are replaced by reorganizing neighboring tissues into whatever parts have been cut off. Animals with more complex bodies usually regenerate parts by producing a specialized bud, or blastema, at the site of amputation. The blastema supplies the tissue necessary for the regenerated part.
The regenerated body part is not always the same as what was lost. Many insects regenerate abnormally small legs from which some segments may be missing.
Tadpole tails, for example, typically grow back to about only half their original length. And regenerated parts often differ in details. A regenerated lizard tail, for example, contains a cartilaginous tube instead of the vertebrae in the original.

Nice answer but you should add some references. Alvadro labs work on S. mediterranea for example.


text:
Do voltage-gated channels in a neuron use ATP
I have a question about action potentials in a neuron.
Do voltage-gated sodium and potassium channels use ATP? I mean when they are closed or when they want to open the gate, do they use ATP?

No, they change conformation in response to voltage. Wikipedia has some general discussion of the gating process, as would any basic neuroscience textbook.
The primary energy (ATP) cost of neurotransmission is in establishing ion concentration gradients, via the sodium/potassium ATPase. You can think of this as a special case of secondary active transport, where the energy costs are in establishing a gradient that is then used for a later process which does not cost any direct energy.

Learning and memory (synaptic weight matrices) are mediated, in part, by the concentration of voltage-gated sodium channels at the neuron’s axon initial segment. The more voltage-gated sodium channels, the more efficacious is the transformation of a neuron’s collective synaptic input potentials into output action potentials. Those voltage-gated sodium channels, dendritic spines, ion gradients, and synapses are continually be built up and broken down depending on the learning needs of the animal. While it is true that the Na, K, and Ca flow down electrochemical gradients when depolarization opens up the voltage-gated ion channels (and don’t use much ATP/energy at that instant), there is an immense expenditure of ATP/energy in the prefatory synthesis of protein, degradation of protein, and pumping ions against electrochemical gradients in order to establish the membrane potentials in the first place. Source: Lou, L. “Principles of Neurobiology” Chapter 10

It's typically ligand-gated channels that change concentration with learning and memory. Voltage-gated channels at the axon initial segment can regulate the transfer function, yes, but this affects all inputs to a cell rather than affecting them directly. In any case, this seems mostly irrelevant to the question asked.


text:
Is there a biological or technical reason for a 40 Ct cutoff in nucleic acid detection assay?
I have developed and validated a modified a nucleic acid test (NAT) for SARS-COV-2 detection using real-time RT-PCR (aka rRT-PCR, aka RT-qPCR). My assay is not for diagnostic use, but for donor screening (which are similar, but different enough to require independent validations). The PCR step is sensitive enough to detect a roughly a single gene copy per reaction, but not always with a sub 40 Ct (which may or may not be an issue).
You see, the protocol is built around the primer/probe sets first published by the US CDC, so I initially adopted the criteria in the CDC EUA protocol, which stipulate a Ct value < 40.00 to classify a target as positive. This means is that amplification with a Ct value of 39.99 is classified as positive, while a nearly identical amplification curve with a Ct of 40.01 is classified as negative. Looking at similar NATs for in vitro diagnostics, most use this same cutoff. It seems fairly common with tests for other pathogens too.
For a little background, using a cutoff like this reduces the potential for subjective classification errors between users by providing a qualitative, binary interpretation for an ostensibly quantitative data readout. The trade-off is that an improperly assigned cutoff can result in systematic classification errors that are universal among all users. Anyone who has used one of the protocols based on the CDC probes has noticed that the two primer/probes sets targeting the SARS-CoV-2 viral genome do not perform equally well. It's common for test results to be classified as "inconclusive" when one viral target is positive, but the other is "negative" because of a Ct value just above the 40Ct cutoff. (I've already tweaked my protocol to reduce this kind of error, but could not eliminate it completely).
As I am writing this up for publication, I'm wondering if it would be better (more honest) to recommend a Ct cutoff that reflects the empirical range of Ct values in my validation studies, as opposed to keeping it at some seemingly arbitrary round number (even if it is almost universal among similar tests). Doing so would not change any of the major findings I report (sensitivity, specificity, etc.), but would change some of the numeric values. More importantly, I think it could help prevent misclassification of late-amplifying samples as negative.
Does anyone know of a biological or technical reason why this cutoff should not exceed a Ct of 40? Maybe this is just some convention that is blindly carried forward; or maybe there's some quirk of TaqMan chemistry to justify this value that I'm just not aware of.

This is done because at some point you start amplifying nonsense and not get a meaningful signal. If (and this is most often not the case) you have the ideal doubling of you DNA template in each cycle, you can calculate how little DNA you start with to detect it only around cycle 40 - or the other way round: What you will amplify and see as a "signal" by then.
If you have templates which always really come this late, I would use more DNA (and probably more RNA to start the rtPCR) until this comes at least 2-3 cycles earlier and then do serial dilutions of your template to see if this signal is real or not. If so, you should see a relation between Ct and dilution.
For doing this you need a negative control which stays really negative until your sample signal shows up - which is tricky on its own because at some point you will see some kind of primer self-amplification. If this occurs in the same range as your sample, your signal cannot be used. If no other primers can be used for technical reasons, sometimes nested PCR has to be considered.
And last but not least all your reagents degrade over time by cycling them 40 times through the PCR program (also the polymerase), which affects the efficiency of the reaction.

I know this applies to SybrGreen assays, where fluroescence is a measure of total DNA present, but with TaqMan chemistry, fluorescence should only increase when both probe and primers match. My NTCs and negative specimen controls never come above baseline over 45 cycles (have run literally dozens of plates at this point).

The signal is definitely real. Have done 10-fold and 2-fold dilution to extinction series in my reference matrix to establish the LOD (20 independent reps per dilution in the 2-fold series). Viral copy numbers quantified via digital PCR. Plus, each sample is assayed with two different primer/probe sets targeting the viral genome plus an internal amplification control. The more efficient of the two viral targets maxes out around Ct 37-38, while the other set lags by ~2-4 Ct (max around 42.5).


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Do circadian hormones fluctuations follow sleeping patterns or the time of day?
It is said that testosterone and cortisol are at their highest early in the morning, at 8 am, and lowest at night.
What happens, though, if someone regularly goes to sleep at 8 am and wakes up in the afternoon/evening over a long period? What happens if sleep times are inconsistent, sometimes sleeping overnight and sometimes in the morning? Do hormonal fluctuations follow the sleep pattern or do they follow the time of day?

I think your question will be better received without the "I" parts of it, so I've edited it accordingly. Additionally, it's good to provide citations for things you read about, so if you can cite where you read about daily cycles of testosterone and cortisol that would be great.


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If you add type A blood to type B blood, is there a visible reaction?
I read that the original discovery of blood types was because they combined random blood samples togethers and noticed a reaction. I was wondering if this was a visible reaction? Or is anti-A or anti-B serum explicitly required?

Blood contains serum too.


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Can alleles have cyclic dominance?
Do the relationships between alleles always form a hierarchy? Ignoring partial and codominance, can alleles have a cyclic relationship? For example, is there anything that exists analogous to the following 3 fictional alleles:
Rock -> Scissors -> Paper -> Rock
If so, it's easy to see what would happen in a diploid relationship and which phenotype would be expressed. But what would happen in a triploid organism? Would nothing be expressed because each allele was dominated by another?

Have you thought about what dominance is caused by?

I understand situations like a pigment being produced or not being produced. But what I'm asking abouot if any boundary conditions exist that are outside the norm. Specifically, modes of inheritance that have non-binary causes.


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Genes are linearly arranged on the chromosome
Could someone please explain the meaning of the statement given by TH Morgan:
"genes are linearly arranged on chromosomes"
Since according to my knowledge there are noncoding parts in between.

Can you give more information about why the existence of noncoding segments precludes a linear arrangement? A linear arrangement of genes could imply the linear arrangement of all the stuff in between, no?

Too long for a comment (But I don't have enough reputation so...) Check the following: 1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1091521/
2. https://s4.lite.msu.edu/res/msu/botonl/b_online/e11/11b.htm#:~:text=Genes%20Are%20Arranged%20on%20Chromosomes,sometimes%20separated%20from%20each%20other.
3. https://www.britannica.com/science/theory-of-linear-arrangement-of-genes 4. https://www.nature.com/scitable/topicpage/thomas-hunt-morgan-genetic-recombination-and-gene-496/ Informative and a good read :)

And have you any idea of when TH Morgan said that? And what the state of knowledge about the chemical structure of the chromosome was at the time?

This combines two important findings to which Morgan's lab contributed.

Genes on the chromosome: They could show that mutated phenotypes were linked to the physical entity of chromosomes.
Arranged linearly: They could show that there are distances between different phenotypes correlated to a specific linear arrangement. These distances correspond to the physical distance on these chromosomes (and thus how frequently they are co-inherited). More specifically they showed that distances suggest that the space is linear,  e.g.: in ---A--B-------C-D-   , A would be commonly inherited with B, but less so with C, and even less with D ... ; Theoretically one could have also thought that the chromosomes are circular (as they indeed are in some bacteria) or adopt an even more complex shape, e.g.: some net-like meshwork on which mutated phenotypes / genes sit. In these other cases one would anticipate more complex patterns of co-inheritance among all pairs of genes relative to a linear arrangement.

This is a very good answer and I'd like to upvote it, but it doesn't have references. Please help by adding them. :)

@David I wasn't the one who posted this question!

@Adhish Whoops. Sorry.


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How do crickets get away with being so loud without getting eaten?
How do crickets get away with being so loud without getting eaten? There are a number of bugs that reproduce by blatantly advertising their location. For instance fireflies advertise their location with physical light and are extremely easy to catch.
How is this evolutionary selected for?

For loud calls to be stable in large-population evolutionary dynamics, the fitness benefit from the call (e.g., mate attraction) must exceed the fitness costs from the call (e.g., predator attraction).
Individual species can 'solve for' benefit > costs by any number of devious tricks. One classic trick used by noisy insects (e.g., cicadas) is 'predator saturation'. Imagine you're a predator that hunts noisy insects by following their call - any time you find one, you'll eat it - unless you're already so full that you literally can't fit any more insects down your gullet. If the noisy insects have a short breeding season, and are noisy for the whole of that season, then during the season you will very quickly fill up and be unable to eat, but you will only have eaten a tiny fraction of the insect population.
If the predators are already full, the costs of predation risk are very low. The benefits of mate attraction remain as high as ever. In that case, an insect's best strategy is to sing as loud as possible.

Periodical cicadas are a great example of a noisy prey species with a remarkable predator satiation strategy.

Do you have some citations to go with this answer? Studies which have experimentally / theoretically shown that theory explains what we might see in nature.

Your explanation of cost/benefit ratio is spot on, but I'm not sure if predators 'being full' is that applicable in nature since that would just increase the predator population. It probably has more to do with relative risk of predation (i.e. it's not that the predator is so full that it stops eating, rather, the predator is just eating your neighbor instead of you).

@etis You're right, I simplified some of the details. Predator saturation also requires that the predator population doesn't grow to the point where it can eat all of the saturating prey: predator populations must be limited by something other than peak prey abundance. Fortunately for the cicadas, there are eleven months per year where their predators aren't stuffed to the gills, and the food supply in those months are what limits the predator population.

@bshane That definitely makes sense for the cicadas that all emerge and call at the same time. Do you think it still holds for crickets that call consistently throughout much of the year?

@etis re: 'being full'; formally, I should have talked about 'prey handling rate', which incorporates the rate at which predators can find, catch, handle, and digest prey. I don't think the distinction makes much difference in practice - there's still a point at which the predators just can't keep up with the sheer volume of prey.

They don't always 'get away with it'!  A study by Pascoal et al. (2014) found that field crickets (Teleogryllus oceanicus) on Oahu and Kauai islands of Hawaii have lost the ability to produce sound after an invasive wasp that is acoustically oriented to prey was introduced to the islands within this century. There are a few mutation to the crickets' wing morphology that produces "flat wings" that cannot make sound. Ordinarily, this mutation would reduce fitness through a reduction in competition for attracting mates. However, the selection pressure from the wasp caused independent mutations for flat winds to sweep through the island to the point that the Kauai population was 96% flat wing.
This example illustrates that the deciding factor between 'getting away' with producing so much noise comes down to the selection balance of attracting more mates or attracting more predators.
Reference:
Pascoal, S., Cezard, T., Eik-Nes, A., Gharbi, K., Majewska, J., Payne, E., … Bailey, N. W. (2014). Rapid convergent evolution in wild crickets. Current Biology: CB, 24(12), 1369–1374.


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What kind of mushroom is this in central Europe?
I found some mushrooms in the forest and I'd like to know what kind it is, for being able to tell how to protect the trees from it.
Growing Info
growing location: central Europe, forest
host plant: beech tree, alive
season: late Summer (Sept. 15th 2020)
The area where the mushrooms were found is a typical beech forest with unusually low water levels, as the last few summers have been drier and warmer than usual. I presume the trees suffer more from these mushrooms because the trees are weakened due to the hot weather and little rain.
Some of the mushrooms dry out while on the host tree.
Picture Taking Conditions
The closeup pictures were taken at home. This was after transporting the mushrooms and storing them in the fridge for 2 days. They got a bit squeezed during this procedure.
Pictures
host tree:

host tree from below:

multiple mushrooms, pic A:

multiple mushrooms, pic B:

bright mushroom, pic A:

bright mushroom, pic B:

bright mushroom, pic C:

cream colored/older mushroom, pic A:

cream colored/older mushroom, pic B:

cream colored/older mushroom, pic C:

Based on the lateral stem, fan-like shape, and growth on wood, I believe these are Pleurotus or a closely related genus. Pleurotus are generally soft, while Hohenbuehelia are more rubbery (David Arora, Mushrooms Demystified, 1986). Telling the species definitively will be more difficult, though they do resemble P. ostreatus, which grows throughout Europe. A number of similar species are difficult to tell apart.

Fig. 1. Pleurotus ostreatus. source: iNaturalist
P. ostreatus is only weakly parasitic, which suggests to me that the beech may be already dying from the stressors you mention. A professional silviculturist would be able to make recommendations for forest management.

A professional mycologist would say: As a general rule, you need 4-5 identifiers of a non-confusable species to be safe. So rule 1/ Check if there are any species in your region that can be confused with pleurotus. Compare the size. Check the aroma, the cross section compared to pleurotus, and do a spore print color if you are not sure of yourself. Most people would say they are pleurotus to a very high degree of probability.


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What phase of Action Potential (AP) exactly defines the Relative Refractory Period?
I am posting below, word for word, two statements made on Relative Refractory period - the first from the text: Human Physiology for Medical Students by Magdi Sabry, and the second from a web page with the URL:
https://content.byui.edu/file/a236934c-3c60-4fe9-90aa-d343b3e3a640/1/module5/readings/refractory_periods.html.
In addition, I've attached a photo from Google which appears to be in support of the second statement.
But which of these is correct?

"Relative refractory period (RRP)...corresponds to the remaining part of the descending limb of the AP till the start of after-depolarization (i.e. during the later 2/3 of RP)"

2."...there are two types of refractory periods; the absolute refractory period, which corresponds to depolarization and repolarization, and the relative refractory period, which corresponds to hyperpolarization. "

By "AP", I assume you're referring to action potential? (I'm not a neurologist)

Yes, I mean Action potential, and I've edited the post.

Neither is an accurate definition; both are correct and not conflicting if you interpret "corresponding" to mean "typically/approximately corresponding".
The absolute refractory period is any time in which you cannot evoke another action potential no matter the strength of stimulus, due to an action potential in progress/that has just occurred.
The relative refractory period is any time in which you can trigger an action potential but need a stronger stimulus than normal.
Neither of these definitions refers to specific phases of the action potential in terms of voltage or change in voltage. Yes, typically the absolute period includes the ascending and descending phases of the AP, but there's no reason it can't last longer depending on the gating properties of the sodium channels. Similarly, the relative refractory period starts with the end of the absolute refractory period and continues through the hyperpolarization phase, but there is no reason it cannot end sooner or later, again depending on gating properties.


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Evolution of Heteromorph Ammonites
I was reading about fossils and thought of this question: what was the purpose of the shells of heteromorph ammonites (for example, ammonites of the genus Nipponites)?
Wouldn’t the odd shapes of these shells cause more drag? So why did their shells evolve to be that way?

Some jellyfish travel with currents and tides, so the nipponites can travel further with more drag if the use currents. Crioceratites have an open spiral which makes sense, if they turn sideways they can travel faster than an typical ammonite with the currents, and if they turn edgewise they are about the same. Cool question it's a very complex biophysics and geometry topic.

I'm not an expert in functional paleontology, but it has been suggested that the specific shape of heteromorph ammonites could be related to hooking on to macrophytes or branched animals:

Examination of ribbing pattern and its resolution in various parts of
the living chamber in 11 species revealed that the ribs were less
developed and had some traces of wear on the inner surface of the
hooked chamber, being well developed both on the lateral and outer
lower parts. This could indicate that the adult animals were
semi-loosely hooked (Ancyloceras, Macroscaphites) or permanently
clipped (Scaphites, Hoploscaphites) onto either horizontal or upwardly
angled stipes of non-calcified algal macrophytes or branched animals.
Comparison of the adult mode of life with those of modern cephalopods
suggested that ammonites of the suborder Ancyloceratina had developed
a stationary brooding phase that could have several ecological
advantages over free-swimming monomorph ammonites.


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Optimal agriculture: maximum yield with minimum environmental impact
I read more and more stuff about alternative method of agriculture such as permaculture. Howerver, I'm not an ecologist or biologist so I don't know where to look for really good and serious articles / paper on the subject. I am really interested in food production methods that may be efficient and respectful for both the environment and the health.
The question that interests me the most is the question of crop yield and environment. I wonder if there are studies that compares the crop yield of the different production methods AND if there are scientific researches on the optimisation of the food production under ressources constrains.
Do you have any reading suggestion? I'm mostly interested in scientific papers but I'm open to anything that may be interesting.

Google Scholar is often a good place to start your searches. Start big (broad topics, review papers), and work your way into more specific topics as you learn how different terms are used in scientific publishing. You may not be able to access certain (probably most) literature without institutional credentials, but you should at least get to a summary/abstract page, and you can always try SciHub for the full text (I'll let you figure out how that one works).

Publications by the Food and Agriculture Organization http://www.fao.org/documents/card/en/c/ca9692en of the United Nations would be a good place to start as they are freely accessible. There are plenty of articles looking at crop yield of different production methods and different management techniques. You may consider subscribing to a journal, like Agronomy https://www.agronomy-journal.org/, or CAB Abstracts https://www.cabi.org/publishing-products/cab-abstracts/ as those would contain most of the subject material you're looking for. Those would also contain information on optimizing food production under resource constraints. Happy researching!

Welcome and thanks for your post. Can you add links to websites or add other linked resources in your answer to enable other users to check out your suggestions more easily?

I believe you are looking for information on "sustainable agriculture". There are many aspects of production in agriculture like: fertilization, irrigation, pesticides and (no-)tillage. One can try to calculate the carbon foot-print of food (beware of the calculations, they might be misleading).
Crop rotation is helpful in sustainable agriculture but it is not always available, making  traditional (industrialized) agriculture the only viable option. The economic aspect is also important. Agricultures need to grow the food and they will grow it only if the make money from it. Organic and sustainable agricultural products get a premium for being cultivated that way but these premia go down as more farmers use them.
The question "How the yield is affected by the agricultural method" is a broad question that attract interest in research. We need to break it down to: What is yield (biomass? marketable product?) and what is agricultural method.
A great study conducted in Ontario, Canada by Stonehouse et al, 1996 compares the herbicide treatments in 3 types of farms: conventional, reduced input and organic and the yield, investment and profit for three crops: grain corn, beans and cereal grains. The data arrives from self-reported data by the farms. This is not a fully randomized experiment and there are many differences between farms (size, investment, land) but precautions were taken to reduce them. Reduce input farmers used less herbicides than the conventional ones.
This is the table from the article

There reported more information as profitability but since this study is from 25 years ago I believe it is no longer relevant.
This study is only one showing the complexity of the subject and one of the methodologies employed. One can write various books about the subject so I hope this post gives you the direction that you needed


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Help identifying organism
I would like help identifying this "crab".
I looked through 32 pages of crabs on this resource http://species-identification.org/ but none of them look like this little animal found in the waters of Madeira.
They move fast and are something in between a spider and a crab.

It is definitely a crab - not anything spider. I originally thought it was a Sally Lightfoot Crab (a common crab on Madeira from the family of shore crabs) but I agree on your comment that it is more likely a Nimble Spray Crab (of the Flat Crab genus) as the specimen in your photo seemed a lot flatter than a shore crab (but I wasn't sure if it was just the shape of the rock).
The Wikipedia article on this species says that these are also referred to as another kind of Sally Lightfoot crab, and the fact that these are in a different taxonomic family from the other ones (the shore crabs) is a topic of debate.

They are observed in the coastal Atlantic and considered native to Madeira, but have recently spread into the Mediterranean

You can view a gallery of almost 200 photos of these crabs on iNaturalist.

According to my dive instructor and to these pictures: https://inaturalist.ca/taxa/61372-Percnon-gibbesi/browse_photos it indeed is a kind of Sally Lightfoot, specifically it's the Percnon Gibbesi (Spray Crab). Thanks. If you edit your answer to reflect this I'll accept your answer.

Thanks for the clarification - edited to reflect your feedack


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Do we come to know which allele is dominant by seeing family genration tree only?
I know that a Gene has Alleles (variation) and one is Dominant over Other i.e the Other Recessive.
Then I got a Thought that How can we tell whether an Allele is Dominant or Recessive...... and I came across this Site while Googling, and It says we can tell this by Observing Patterns in the Family Generation Tree.
So, my question is that can we only describe an Allele by observing pattern? Is there any other Method or by looking at the Molecular level and tell?
Please extend this "How can we tell whether an Allele is Dominant" to a Special Case where a Gene has 3 Alleles.....can we have 2 Dominant Allele?

Addressing Your First Question
We can tell whether an allele is dominant or recessive based on patterns in family trees, that is true, and it is very helpful! However, that is not the only way, since by looking at the molecular function of the alleles, the dominant and recessive relationship between alleles can be assessed without needing to look at family trees!
I think a deeper understanding of what it means to be dominant versus recessive would be helpful, because usually biology isn't just that simple! In most scenarios where there is a distinct recessive and dominant trait, it is because the dominant trait causes some specific activity/functioning protein while the recessive trait does not. Let's look at an example of this:
Let's choose eye color:1
There are multiple genes that affect eye color but let's just look at one: the one that codes for the brown pigment (melanin) to be produced in the iris [specifically the HERC2 gene]. As you probably already know, brown eyes are dominant and blue eyes are recessive.
Let's call the dominant allele B and the recessive allele b. The only way for blue eyes to be the phenotype is for the allele combination to be bb. Now think about why this would occur on a molecular level. Alleles are just forms of genes, which then in turn code for some protein. Think back to what we said earlier about how most of the time dominant alleles cause some certain activity within the cell and recessive alleles do not. We can now use that knowledge to uncover the molecular basis of this eye color scenario: The B allele codes for the brown pigment to be produced in the iris, while the b allele codes for a dysfunctional protein that does not lead to melanin being produced, leading to a blue-ish color seen. So, if the B allele causes the production of melanin and the b allele does not, it makes sense by the B allele would be dominant in this case. In the case of Bb, melanin is still being produced (even if it is because of just one allele), so there still would be brown eyes! Therefore this makes sense by bb is the only allele combination that results in the blue-eye phenotype, because it is the only combination with no allele still producing melanin. This is why brown eyes are dominant to blue eyes, because blue eyes can only exist without the presence of any B allele.
So, by knowing how an allele actually functions on a molecular level, that can help us to understand if it is in fact dominant or recessive to another allele. We should also acknowledge that genes do not necessarily need to be in this black-and-white relationship of recessive or dominant. There is also incomplete dominance and co-dominance!
Now to Your Second Question
When talking about three alleles, it is important to understand that allele dominance only is used when comparing one allele to another allele. So with three alleles, the dominance, recessiveness, co-dominance, or incomplete dominance is between two of the alleles.2 So if we are talking about alleles A, B, and C. We could say things such as:

A is recessive to B, B is dominant to C, C has in-complete dominance with A, etc...

However, it is really up to the molecular function of each of the alleles and to determine how those interactions would take place. But to answer your question directly of "can we have 2 dominant alleles," the answer is sort of. Allele B and C can both be dominant to allele A, but that says nothing about the interaction between Allele B and Allele C.

1 This is a simplification of the actual molecular mechanism of eye color, but at a simplified level this works to illustrate our point. You can read more into the genetic/molecular basis of eye color here.
2 This article is very good at discussing alleles and clarifying the point that dominance is only between two alleles.


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Natural Toxins and Medicine
How are natural venoms and toxins (e.g. spider and snake venoms) used to make antidotes? In other words, what is in that venom that is part of a harmful substance but, when used correctly, can actually help us, and why can these molecules help or harm in different situations?
Also, why are we looking to natural toxins to produce new medicines instead of synthetic chemicals we could make or already have?

You are probably thinking about antivenom using immune serum.
You give the venom to a host animal to induce an immune response, and then purify (to the extent possible) antibodies collected in serum from that animal, and then inject these to the patient to neutralize the venom. You don't use the venom directly.
Isolating components of venom could also allow for screening for molecules that will bind to them strongly and possibly block their action, though I'm not aware of specific antidotes that have been produced this way.


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Why is my DNA band bulging?
This is the only image my the TA was able to get for us. And, we're using it for our lab report. The image isn't even ours. It's another group's image that we're sharing. But I don't understand why in the first lane there seems to be some bulging/ tapered form of the ladder? Can someone explain why has this happened and how? I am very confused...

Band distortion can be caused by any number of things. In my experience, everyone has their own their own guesses about the cause and their own little tricks to fix it. Sometimes the gel sets unevenly, or the loading buffer isn't mixed right, or the running buffer isn't at just the right level, or the dye was expired, or the power supply voltage fluctuated. Sometimes an impatient TA changes the settings mid run to speed things along. Whatever the cause, I wouldn't worry about a little distortion as long as you can see your band and it's approximately the right size on the ladder.

Sometimes molecular techniques can be as much of an art as a science. Just wait until you start doing Western blots.

Thank you for your answers! It makes much more sense.


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What is meant by [protein name]+/- (ie "Myod+" and "Myod-")
I have read a paper where this notation for protein names is used:

Myod+ and Myod-

(or another example, Myog+, Myog-).
What does this indicate?  In the paper I'm reading, and some brief googling, it seems that Myog is itself a protein, and not that there are two kinds called Myog+ and Myog-.
Examples are here (the one I'm reading) (Figure 6c), or here (page 3, pdf page (journal page 958)).

The paper you linked is not open-access, so many people won't be able to help you. However, as a common convention, ProtX+ and ProtX- typically refer to cells, tissues, or individuals that either express or don't express a particular Protein X.

Oh okay, that makes sense.  Thank you.  Sorry I didn't realize it wasn't open source.  It looks like the second one is available though (if I open in incognito, I can access)

To expand on @MattDMo , italicized names indicate genes, with the + or – being used to describe either genome or cell with or without an active copy of the gene and thus able to make the protein, the name of which may or may not be the unitalicized form of the gene. (Many genes are named for the phenotype they convey or some other reason when they are discovered before the protein product has been identified.)

@David or.......

@MattDMo either of those could make a concise answer. Probably not a lot of reference needed for an answer like this; one example might be nice but not really necessary.

@MattDMo — Do you want to follow up Bryan’s suggestion?

@David I did...

@MattDMo — Good.

The Stem Cell Reports paper linked in the question is open-access, so anyone can download it freely. Unfortunately the Nature paper is not.
There are two different abbreviation conventions being used in the open paper – MyoD+/MyoD- and MyoD+/MyoD-. The italicized version indicates the genotype of the cell, tissue, or individual being referenced, so for example MyoD- indicates the MyoD knockout they made. This convention is very widely used to refer to genes or mRNA.
Examples where the gene name is not italicized refer to the protein product of that particular gene and its presence or absence. So, MyoD+ cells express the wild-type protein, while MyoD- cells do not. This convention is also very widely used to refer to the presence or absence of the indicated protein.

Are there rules on the site against me sharing the part of the figure I am talking about (that is not open access)?

@user8243 it may be copyright infringement, but I'm not a lawyer.

I think my smaller question doesn't require it.  Reading through the methods, it seems all of their cells are from embryo sample, and no genes were explicitly knocked out.  Then here, does the minus indicate that no expression was observed?  Seems like it follows from your answer, but wanted to check

@user8243 the minus can either be used to describe a KO ("no expression is expected"), or to describe the results of an assay where expression is actually tested, such as immunofluorescence or Western blotting.


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2nd messenger mechanisms
Many hormones use 2nd messenger mechanisms, such as cAMP and cGMP, and also act on the same cells. For example calcitonin and PTH both use cAMP and have opposite effects.
How is it possible that the same second messenger molecule (cAMP) can have opposite effects on the same cells? Why are there more hormones compared to 2nd messengers - doesn't that reduce the uniqueness of each hormone? Shouldn't that make the function of any hormone using e.g. cAMP be the same as that of any other hormone using the same 2nd messenger on the same cell?

Yes. Got it! Thank you!


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Where are the ATP synthases synthesised?
The nano-machinary of energy production ATP synthase is well known to exist on mitochondrial inner membrane and chloroplasts. But how and where are they formed or synthesised ?

Welcome to SE Biology. Please read the Help on asking questions, where you will see that you are expected to show the research you have done before posting. Have you searched for ATP Synthase or Synthesis of Mitochondrial Proteins. There must be Wikipedia entries on this topic.

Sorry that I have no such things to add. I'm only a 12th grade student just interested in the topic. Thank you for the advice , I'll try to improve the way I post questions.

Yeah : ) questions don't even end there. One can go on and on endlessly to new levels of understanding. I would definitely be delighted to feed my 'what's next's but  it's inevitable after a certain level there will be none to answer. That doesn't curb the quest though ;) thank you for finding me those topics !

The interesting thing is that the mitochondrial ATP synthase consists of many subunit proteins, both encoded by nuclear DNA and mitochondrial DNA. It has long been unclear exactly how these synthases are assembled, and what differences exist between bacteria, yeast, and humans - where ATP synthase formation is normally studied. Regardless, each of these proteins is translated on ribosomes from mRNA transcripts of genes, just like regular proteins. However, these must come together correctly (in the right order) and end up in the correct location.
There are recent publications that answers your question rather directly.
Assembly of the membrane domain of ATP synthase in human mitochondria
In short:

We have shown that the assembly of human ATP synthase in the inner [mitochondrial] membrane involves the formation of a monomeric intermediate made from 25 nuclear-encoded proteins into which the two mitochondrially encoded subunits are inserted and then sealed by association of another nuclear-encoded protein, thereby dimerizing the complex. Association of a final nuclear protein oligomerizes the dimers back-to-face along the cristae [inner membrane of the mitochondrion] edges.

A commentary on the paper is also available, which provides insight into the historical and biological context and difficulties which the paper addresses and overcomes. It may be worth reading their synopsis first. You can find it here:
Assembling the mitochondrial ATP synthase

I admire the elucidation. Thank you !

And sorry that the question was closed. The mods and voters are quite overly zealous here sometimes. Neither a duplicate nor a homework question. Interesting question, certainly.

At first it somewhat disappointed me too. being a newcomer in SE I had problems understanding a dialogue box, which stated that somone suggested there's something similar to my question out there and asked me if it meets my queries. Finding that question resourceful and interesting I clicked yes and right after that my question turned duplicate . Surprised me ! Anyway, the tiny piece of machine inside our cells is marvelous enough to ignore all that, Thanks :)


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quiescent stage (G0) occurs at the end of M phase or G1 phase:
I know that G0 phase occurs when certain cells exit the cell cycle during G1 phase but that means it goes to G0 phase after M phase right?

Welcome to SE.Biology! It is often helpful to do a little internet research such as e.g. googling your question.
I googled it and it gave me this image, which tells me that G0 cells leave from and re-enter G1 phase.


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Which was the first DNA-based genome to be sequenced?
The Wikipedia article on phi X 174 states that:

The phi X 174 (or φX174) bacteriophage is a single-stranded DNA (ssDNA) virus that infects Escherichia coli, and the first DNA-based genome to be sequenced.

But, the article in Wikipedia on Whole Genome Sequencing states:

The first whole genome to be sequenced was of the bacterium Haemophilus Influenzae

So as bacterial genomes are DNA-based, I am confused as to which organism was the first DNA-based one to be sequenced.

Did you follow up the references for the two claims? Which is the oldest? And are you sure there was no qualification to the second claim.  You can surely answer this question yourself. In any case, you should remember Wikipedia articles are written by anyone. There is no central organization and the only checking is that done by people who are interested. There are other sources of information on the internet.

Another thing to consider is that some scientists (and lay people) do not consider viruses to be true "organisms" as they are incapable of reproduction on their own and therefore not truly alive.

@David yes, but my point was about which was the first organism sequenced - some people may have left previous phage work off the list because they didn't consider them to be organisms or have proper genomes, especially if it's ssDNA. I don't know, I'm just speculating.

I shouldn't have, but it was simpler to give you the answer with links to my sources.

@David, Thank you so much for the answer and I am extremely sorry for so much inconvenience that I caused you . I will try my best to learn from my mistake. Again, thanks a lot for the help.

Expanding the question to the history of the sequencing of genes and genomes in general, I present a timeline taken from a review by Giani et al., entitled “Long walk to genomics: History and current approaches to genome sequencing and assembly”.

The graphic shows how the size of sequenced genes and genomes has increased since 1965, which reflects developments in sequencing technology that are discussed in this and other articles which may be more accessible. It should be noted that the more modern methodologies are not intrinsically more accurate than earlier ones, but can be employed more rapidly.
I see no value in the “Guinness Book of Records” approach to biology, but to satisfy the poster, the genome of bacteriophage φX174 was the first DNA genome to be sequenced (1977), and that of H.influenzae the first bacterial genome to be sequenced (1995). But the RNA genome of my old friend bacteriophage MS2, was the first genome to be sequenced (1976).
And the first human chromosome to be completely sequenced is not on the graphic as it was only published in Nature a few weeks ago (July 2020) — chromosome X.

Postscript
For the record, the quotation from the whole genome sequencing article is actually a caption for a (gratuitous) image of the bacterium, is unqualified, and, thus, is incorrect. But when reading Wikipedia articles it should be born in mind that they are written by people like you and me. Anyone can edit them, and nobody need check them or correct them. Peer-reviewed papers can also have mistakes, but where they are of this type, the referees should pick them up. (But by the time you read this I will have edited the Wikipedia article.)

I understood the part of Wikipedia, thank you for suggestion and your answer helped me to clear all my related doubts within me. And I am truly sorry for so much inconvenience and I  got your point on representing question(Not to use Wikipedia as a reference). Though my question was a weird approach to biology because its not going to come anywhere, I felt satisfied that I am clear with my knowledge because of all help. Thank you so much. Your answer helped me a lot in various aspects. Thank you.


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Ostium: insects circulatory system

What is this? Is this a part of the tubular heart? Does it pump hymolymph? Does it have ostium?

I will alter this answer in response to the poster's comments.
Looking at:
https://genent.cals.ncsu.edu/bug-bytes/circulatory-system/
The diagram doesn't show the digestive system - so no anus.
I see that there is expected to be an ostium (hole) near the end of the heart.
Think about where in the heart the many valves are located, then look at the segments of the abdomen and work out what happens with the heart when the abdomen extends or contracts, which you can see in bees.
What is more interesting in all the diagrams is the decision about whether the heart pumps just to the head, or also through pipes to the ventral region.


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How does transpiration help in sucking water up?
How can transpiration help in sucking water up as the amount of water that is sucked up by the evaporation of water equals to the amount of water evaporated. (Correct me if I am wrong). Then how it helps?

The benefit is not in taking up more water but in transporting the things that water contains.
Plants rely on bulk transport in water flowing though specialized tissue (xylem), somewhat analogous to blood flow in an animal. Water flows through the xylem using capillary action; when water is lost at the top, capillary action pulls water into the vacated space and the flow continues down the entire height of the plant. Water removed for other uses like photosynthesis also contributes, but transpiration is important for many plants to increase the flow rate.


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Why is protein cyclisation desirable?
There are a number of methods to "cyclize" an existing peptide:

Disulphide bond as described in Disulfide Bond Mimetics: Strategies and Challenges by Gori et al.
"Linchpin" based (linker chemistry) as described in Synthetic Cross-linking of Peptides: Molecular Linchpins for Peptide Cyclization by Derda et al.

Why would the "cyclization" of a protein be a desirable goal?

As described in the abstract of Synthetic Cross-linking of Peptides: Molecular Linchpins for Peptide Cyclization by Derda et al., protein cyclization improves:

resistance to proteolytic degradation and conformational stability. The latter property leads to an increase in binding potency and increased bioavailability due to increased permeation through biological membranes.

In simpler terms, a protein that is cyclized is less likely to:

Fold into an unhelpful shape.
Be broken up by an enzyme.

Thus, they are more likely to:

Act as better binders for a given target
Make it across a cell membrane


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Phytophagous worm identification
These worms appear soon after the rain lilies flower and slowly nibble on the leaves growing big and chubby. They are about 5cm long, have many small red legs underneath, have no spines or spikes, and are soft-bodied.
They leave tiny green balls of excreta. I have never seen them metamorphose.  I live in Andhra Pradesh in India. Can anyone tell what species they are? Are they dangerous?

I think it's a caterpillar (an insect), not a worm.

I think you have an Indian Lily Moth (of the genus Polytela). It is considered a minor pest. Their habitat seems to only be around India and its surrounding area.

Their worm matches yours ... smooth, dark, but red patches and white spots:

If you dig in your garden, you may encounter these pupae:

And they eventually grow into these beautifully-multicoloured moths:

Here is a video showing their movements and their life cycle:
https://www.youtube.com/watch?v=2l0oxZM_6XY

But it's quite curious that I have never seen the moths [they look absolutely stunning]perhaps the birds eat the larvae before they turn into pupae?


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Low-cost simple water testing for faecal contamination
I live in Indonesia and there are lots of sewage pipes discharging directly from homes/restaurants/etc directly into the river. It's also common to wash clothes and so on, so there is likely detergent in there as well.
Some water courses that people bathe in seem to be more s**t than water, if you see what I mean, in that it starts off in the river, then diverts into various smaller canals which often end up with trash, diapers, and so on.
I'm wondering what I could do to test/measure this in simple & low-cost fashion, so that I could test in different places and on different dates, and possibly to include quantative values such as 'how much dirtier' the river is when there are many people bathing in it, or when it is dry season, or whatever.
I think I don't need to test for every pathogen so it might be sufficient to just test for E coli? [I think S. aureus is also common, as skin boils tend to occur after bathing in dirty water.]

I don't have a good answer for you, but I'd note that this sort of thing is often a target of international health organizations.

You could start by reading about the presumptive coliform count: https://microbeonline.com/probable-number-mpn-test-principle-procedure-results. I'd also recommend reading a textbook of microbiology/public health for more detail, because this is a standard topic in those fields. An example is: https://www.universitiespress.com/details?id=9789389211436.

The best and most common would be the "multiple fermentation tube” or “most probable number” technique. Rather than testing for all pathogenic bacteria, it uses indicator microorganisms to assess the potability of the water. You'll need a lab to do this but if you have access to one, I'm sure that all the needed materials are common there. Here's a copy of the method: https://www.who.int/water_sanitation_health/resourcesquality/wqmchap10.pdf


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What part, roughly, of the carbon in a plant comes from the soil? As opposed to the atmosphere?
C4 plants contain a slightly higher percentage of carbon-13 than C3 plants. Is this because of carbon obtained from the soil or the atmosphere?
I have read that plants using different chemical pathways, such as millet and wheat, incorporate distinctive proportions of stable carbon isotopes from the SOIL.
Do C4 plants need more carbon-13, or does that process just happen to result in accumulation of more carbon-13?

Always good to cite things you've read.

Does this answer your question? How do plants absorb CO2?

Only a small fraction of plant carbon is soil-derived: e.g. from Majlesi et al 2019:

although the majority of plant C was obtained from atmosphere by photosynthesis, a significant portion (up to 3–5%) of C in plant roots was derived from old soil

(in an experiment with Scots pine and reed canary grass).
As laid out by this review of C4 photosynthesis (Kellogg 2013), the primary reason for differential isotopic make-up of C3 and C4 plants is that the biochemical pathways they use fractionate isotopes differently — not because the plants' requirements are different.

Because of the very different
affinities of Rubisco and PEP
carboxylase for CO$_2$ , C$_3$ and C$_4$ plants
differ in the carbon isotopes that they
assimilate. While most atmospheric
CO$_2$is made up of ${}^{12}$C, a small fraction
includes ${}^{13}$C. Rubisco has a fairly high
$K_m$ and hence low affinity for CO$_2$, and preferentially fixes ${}^{12}$C. The ratio of ${}^{13}$C
to ${}^{12}$C ($\delta^{13}$C) in a C$_3$ plant is thus much
lower than the ratio in the atmosphere;
the carbon in structural and storage
carbohydrates contains much less
${}^{13}$C. PEP carboxylase has a lower
$K_m$ for CO$_2$ than Rubisco and hence
a higher affinity; as a consequence it
discriminates much less against ${}^{13}$C
than Rubisco does, so that the $\delta^{13}$C
is appreciably closer to atmospheric.

Kellogg, Elizabeth A. 2013. “C4 Photosynthesis.” Current Biology 23 (14): R594–99. https://doi.org/10.1016/j.cub.2013.04.066.
Majlesi, Soroush, Jukka Juutilainen, Anne Kasurinen, Promise Mpamah, Tatiana Trubnikova, Markku Oinonen, Pertti Martikainen, and Christina Biasi. “Uptake of Soil-Derived Carbon into Plants: Implications for Disposal of Nuclear Waste.” Environmental Science & Technology 53, no. 8 (April 16, 2019): 4198–4205. https://doi.org/10.1021/acs.est.8b06089.


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What are the carbohydrates that are found in white rice?
From this Wikipedia page on rice, it is mentioned that 100g of rice contains 80 g of carbohydrates, of which 0.12 g is "sugar" and 1.3 g is "fibre". I believe the "fibre" refers to dietary fibres that are not absorbed by the body and are just passed out of the body. However, I understand "carbohydrates" to be almost the same as "sugar" so what is the difference between the two terms as used in this context. I am guessing that "sugar" refers to simple monomeric units of carbohydrates while the rest of the "carbohydrates", excluding "sugar" and "fibre", is in the form of starch polymers, namely amylose and amylopectin. Could someone help to verify my understanding?

Fibre is contained in a particular form of starch, called resistant starch. Fibre, like sugars and starches, is a type of carbohydrate. However, fibre is different because it is not digested by the human body in the same way as sugars and starches. this is a good read from the 4th paragraph: https://www.researchgate.net/publication/305890780_Rice_as_a_Source_of_Fibre

The word carbohydrate is most common in biochemistry, where it is a synonym of saccharide, a group that includes sugars, starch, and cellulose. Starch (a polymer of glucose) is used as a storage polysaccharide in plants, being found in the form of both amylose and the branched amylopectin. In animals, the structurally similar glucose polymer is the more densely branched glycogen, sometimes called "animal starch".

@aliential you might consider putting your comments as answers instead, as they seem to actually answer the question rather than comment upon it.

Thanks, its just copy paste research...


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Why are lungfish cartilaginous?
Lungfish have a cartilaginous notochord, and a reduced cartilaginous skull. Is this feature to improve flexibility, or is there another reason?

Your question is interesting and relevant to here, but it's expected that you show you have researched and tried to find answers to your question before you post, rather than expect others to do it all. Could you include it in your post?


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How to approach identifying Melampsora species?
I'd like to figure out which species of Melampsora that is growing on this European aspen. What would be the right approach? Would a microscope or other tool help? Is there even more than a single species that attacks aspen?
These photos were taken of an aspen leaf in Stockholm.


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COVID-19 deaths by year of birth?
Are there (global, country, etc.) data of COVID-19 deaths (or hospitalization) by year of birth? I was able to found them only by "age group", the meaning of this being usually an interval of 5 to 15 years, but I'm interested in smaller intervals.
Why I am interested? We know that the severity of this illness increases with age, and in fact increases a lot with ages around 70. If this increasing is more o less locally constant (that is, the first derivetive does not vary much in any interval of a few years) or at least the second derivative is more o less locally constant, we can think that maybe age on its own is a factor risk. But if there is a rapid increasing in one, two or three (consecutive) years and then a smaller slope (that is, a sort of "jump"), it is possible that there are (instead/also) other factors: maybe an exposition of this aged people to something during their lives that younger people don't lived, or some other thing that we don't know yet. So we need to know with more detail ages of hospitalization, deaths, or other sign of severity.

Data are usually binned in broad age groups partly because that's all the detail that's useful in some context, and because access to more detailed data often involves access to strongly controlled, personally identifiable information.
This preprint (full disclosure: I'm a co-author) gives information in 2-year bins for COVID in Ontario, e.g. this graph of the fraction of known infections (KI) hospitalized, and fraction of hospitalizations that resulted in survival, by (2-year) age group.
It looks pretty smooth, although if you squinted hard you might be able to convince yourself there were some breakpoints, e.g. between [60-61] and [62-63] in hospitalization or between [62-63] and [64-65] in survival (although I doubt these impressions would stand up to a formal statistical analysis ...)

Thank you. Indeed these curves seem pretty smooth. There is another break (in hospitalization) between [68-69] and [70-71] (of a different nature, since it is preceeded by a higher slope) but this one seems very small in the curve of deaths in the preprint. Very interesting paper!


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Giant insects growing question
During the dinosaurs time 100-200 million years ago there were giant insects like 1 meter long. An example is here. One of the theories why they could grow this big is that oxygen level was much higher than now. Now we have like 20% oxygen in the air and that time it was 30 or 40.
The question:
If I make a tank/aquarium with 40% oxygen and all the equipment to make this oxygen concentration constant. I put there modern insects, dragon fly, worms, slugs, etc. Will they grow to much bigger size than normal from the 1-2 generations, or I will need to have 100 or 1000 generations before they will be bigger?

This has been done in insects at least: https://jvandenbrooks.wordpress.com/research/

You would need some sort of factor that selects for a larger size.  This isn't impossible, since humans do selective breeding for size in animals (e.g. St. Bernards and Chihuahuas) and in plants.  I don't know of any selective breeding of insects (maybe honeybees?), but I'm sure it could be done.

that sounds like a fun experiment!  But unfortunately you are right, the size difference is shaped by genetics as well as an environmental condition that might be hard to pin down.
For the genetics, It would indeed take millions of years (or at least 100,000s) for the genetic adaptation to kick in to create that change.
As for the environmental conditions, another source of gigantism is being on an island.  As the small number of species expand to fill out all the niches in the tank, they may get larger simply because the environment allows it with no predators.
The tank would have to be enormous to get those niches I think. This paper describes an archipelago of islands and shows that you tend to get smaller animals more easily with smaller islands, and larger species need larger islands.  Large here is millions of square meters.
Both of these processes take many generations. This is not my field but this paper studied 200 generations of plants and showed only migration and lifespan changes.  Size adaptations that come with changing ecological roles might have to take 1000s of generations. We'd have to freeze ourselves to see the giant slugs.  I'm sure there's a better answer out there, but this is what i found so far.

was richard nixon frozen in time?


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How is silica transported to the leaves of genus Dendrocnide trees to form stinging needles for toxin delivery?
I just read the NYTimes' This Tree’s Leaves Look Soft and Inviting. Please Don’t Touch Them. which mentions the genus Dendrocnide and that Wikipedia section begins with:

Contact with the leaves or twigs causes the hollow, silica-tipped hairs to break off, penetrate the skin and inject the toxins.10 The hairs cause an extremely painful stinging sensation that could last from several hours to 1–2 days, recurring to a lessening degree for several months or more whenever the area is touched, exposed to water, or subjected to temperature change. The injured area becomes covered with small, red spots joining together to form a red, swollen welt. The hairs are also believed to be released to the air when the plant is cut or cleared in large areas. Workers without respiratory protection have reported sneezing, runny noses, mild nasal bleeding and throat irritation while cutting or clearing.
10Hurley, Marina. "'The worst kind of pain you can imagine' – what it's like to be stung by a stinging tree". The Conversation. Retrieved 2020-03-08.

and that article says:

The stinging hair structure is complex and consists of a tip, shaft and bulb composed of silica, calcium carbonate and calcium phosphate.

Reference 5 in Neurotoxic peptides from the venom of the giant Australian stinging tree (open access in Science) is Stinging hair morphology and wall biomineralization across five plant families: Conserved morphology versus divergent cell wall composition and this article contains a lot of information, for example following Figure 2:

Biomineralization
Notable differences were found in the mineralization of stinging hairs. Three zones of the stinging hairs could be distinguished based on their mineralization patterns. The tip regions were generally strongly mineralized with highly concentrated silica or calcium phosphate, except for Cnidoscolus stinging trichomes, which were completely nonmineralized. The shafts were usually mineralized with calcium carbonate, but in some cases with calcium phosphate or silica besides calcium carbonate. Trichome bases showed more irregular mineralization, mainly with calcium carbonate and often additional silica deposits (Fig. 2K, L), or they were not yet completely mineralized (Fig. 2M).

This article primarily addresses structure and morphology, but I'm interested in how silica actually makes its way into a leaf structure. Unlike calcium and phosphorous, neither elemental silicon nor SiO2 readily dissolve in water, so I'd like to ask the following:
Question: Presumably it comes from minerals in the soil, but is it transported as particles of silica, or molecules of SiO2, or by other chemical forms containing silicon and reformed as silica on site, or something else?

I don't see a tag related to transport, and I don't think nutrition applies. Is there a catch-all tag for stinger structures or the mechanical aspects of stinging mechanisms?

Biosilicification is a good search term to use.
The silicic acid present around the roots can be actively transported into roots, and later into specific cells or cell compartments. It is deposited preferentially onto lignin or polysaccharide surfaces.
For free articles giving an overview there is:
Nawaz, Muhammad Amjad et al. “Phytolith Formation in Plants: From Soil to Cell.” Plants (Basel, Switzerland) vol. 8,8 249. 26 Jul. 2019, doi:10.3390/plants8080249
found at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6724085/
and:
"From biosilicification to tailored materials: Optimizing hydrophobic domains and resistance to protonation of polyamines"
David J. Belton, Siddharth V. Patwardhan, Vadim V. Annenkov, Elena N. Danilovtseva, and Carole C. Perry
PNAS April 22, 2008 105 (16) 5963-5968; first published April 17, 2008 https://doi.org/10.1073/pnas.0710809105
found at:
https://www.pnas.org/content/pnas/105/16/5963.full.pdf
Keywords silaffins, frustulins, pleuralins (used by diatoms) silicatein (used by sponges)

+1 already :-)


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Presynaptic inhibition
For presynaptic inhibition, I am aware of these:

Ca²+ influx (into the presynaptic nerve terminal) is decreased. And this in turn reduces the probability of releasing synaptic vesicles from the presynaptic neuron.

The influx of Ca²+ is under the influence of voltage-gated Ca²+ channels.

My questions:

What inhibitor(s) can be involved in this inhibition?

What is the ionic basis of this inhibition? (By this, I want to know how the movement of ions affects the voltage-gated Ca²+ channels)

Does the reaction cascade intitiated by the inhibitor in any way affect the amplitude of the AP generated upstream when it reaches the presynaptic nerve terminal?


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What are the differences in ultrastructure of cilia and flagella?
Cilia and flagella are aimed for similar perpose, motion. And both of them show the (9+2) microtubule arrangement. They are nearly identical in structure. But to be more specific , where exactly does the little difference lie (except the 5-6 bridge) ?

Perhaps you mean that flagella spin to provide locomotion whereas the cilia tubules themselves beat. the flagellar motor vs the fixed anchored structure of the cilia...

Thanks for the help but the question actually asked about the difference in their 'ultrastructure' or 'micro-anatomy' you may say...

Eukaryotic cilia and flagella are identical in ultrastructure.
The only reason for two different terms for the same thing is historical usage. Traditionally, 'cilia' has been used for shorter, more numerous structures and 'flagella' for longer structures which are fewer in number.

Although cilia and flagella are the same, they were given different names before their structures were studied.
Source: Lodish et al (2000)

In fact, some have suggested doing away with this dual terminology, and simply calling all these structures 'cilia'.

But isn't there at least some subtle difference like the 5-6 bridging bond in flagella that is absent in cilia ?

@Sarika I am not familiar with that... Can you please share a source for this information?

Thank you for asking me for source! That finally cleared everything :) as I thoroughly looked up once again and found out that both cilia and flagella do contain that '5-6 bond'. I'm sharing the link here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468612/


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Flatworms sexual reproduction; one must be the mother and the other the father?
I watched this.
I wonder if both of these flatworms ever end up pregnant.
Earthworms are simultaneous hermaphrodites, meaning worms have both male and female reproductive organs, just like flatworms. During sexual intercourse among earthworms, both sets of sex organs are used by both worms. If all goes well, the eggs of both of the mates become fertilized. Can this occur in flatworms?
Or in flatworms, one must be the mother and the other the father?


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Are there any examples of predators that ambush scavengers?
I'm specifically asking about animals that use a hunting strategy revolving around hanging around cadavers to attack animals attracted to the cadaver, or even leaving part of their catches out to lure scavengers.

Saltwater crocodiles in Australia are reputed to do this; storing meat under water and later eating the fish and crustaceans that are attracted.
Having trouble finding a good source for this.
Article from national news service below.
https://www.abc.net.au/science/articles/2004/01/15/2045125.htm
Feel free to add references if you can find them.