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Can 1.5 gigabytes encoded in the human genome really account for the complexity of a human being?
I read the human genome is 1.5 gigabytes in size. Thats actually not a lot; Photoshop probably takes more space. Mac OS takes 10+ gigabytes of space. Also, the genome is 1.5 gigabytes when counting base pairs as the alphabet, but the actual unit of information is a codon, which is made of 3 base pairs. That means that if the 64 codons are the alphabet, then the amount of information is (top of the hat calculation) 0.5 gigabytes. This is analogous to a "byte" in computer memory, composed of 8 bits. Byte -> codon, bit -> base pair.
Nevermind that some codons are start/stop signals and not part of a protein defining instruction. You can go further and say that the next level, formed by all the known proteins/chains of aminoacids, is a subset of all possible combinations of aminoacids, and forms a new alphabet. The language of proteins.
Anyway, a cell has 100 trillion atoms, and that structure is controlled by DNA containing 1.5 (or 0.5 depending on taste) gigabytes of instructions. That right there is pretty impressive. But then, the human body has 37.2 trillion cells, and you are telling me those 37.2 trillion cells, each containing 100 trillion atoms, are controlled by ~1 gigabytes of instructions? That doesn't add up.
In computers everything is 0 or 1, but after many layers that simple alphabet of {0, 1} can represent complex structures. I guess the same is possible with DNA, but I feel you'd need way more instructions to represent even the most basic of organs. So, I think I am missing something here. For basic structures, like tissue, veins, eyes, blood, hair; things that we share with animals, is that all encoded in DNA?
The complexity is rather enormous for a rather tiny amount of instructions, so there must be something else controlling organ and bone structure.

@user1136 this article suggest Junk DNA might not be junk after all: https://www.futurity.org/junk-dna-1728712/

The genome is not a set of blueprints, it's more like a set of general rules for growth that are given to a machine.  You also need a "mother' (or an egg or seed) to carry out those instructions.  It's instructive to consider L-systems, and how very simple rules can reproduce the growth of many creatures.  See e.g. and related works: https://en.wikipedia.org/wiki/The_Algorithmic_Beauty_of_Plants

Your question doesn't really seem like a question but an expression of disbelief. Biology is quite incredible so perhaps you can try reading some books on modern genetics and physiology.

Size of any "instructions," be-it in computer programming or biology, is a poor indicator of "complexity," if at all. The plant Paris japonica's genome is 50 times that of a human, I'm not sure which would you consider to be more "complex," or to what degree. In programming, Photoshop CC is 1.3GB in Windows but 800MB on Mac, and yet they function more or less identically, despite the almost 50% difference in size.

This is a VERY hard question to answer; I think mostly because it is very hard to think about how the DNA actually encodes information.
The first important thing to note (and also the only direct answer I can give to your question), is that

(Yes) the human genome does encode all information to make a human being, but only in the context of a cell/organism that can read this genome.

Transferring this to the computer code analogy this means that if the genome is the source code for a program (or rather a couple of them), then the operating system (and also the actual hardware) that executes this code is the cell itself and the two parts have to match up in order to work together.
This is essentially a hen/egg problem: without the cellular machinery to read and operate on the genome the organism doesn't work, but at the same time the genome is the source of the everything that reads it.
If one would put the human genome into another (not closely related) species (or the egg cell of one), this would not form a human being, because the organism/egg cell can't read the instructions properly. (This is also the reason why hybrid animals like i.e. mules are often sterile - the genomes of their parental species are similar enough to be readable and make a working animal, but there are already enough differences to introduce problems).
This brings me to what i think is the actual core of what you're asking:

How can so much complexity be encoded in so little space/bits/... ?

and I don't have a clear answer for that (and neither have I ever seen one). There are, however, a few things one needs to consider
Emergent behavior is when seemingly very simple and limited rules lead to very complex structures. This happens all the time in nature and our body plans are no exception, it is however very hard to see or understand and even harder to consciously design from scratch. Nowadays, machine learning algorithm can get complex results from initial simple instructions, but only because they run 'a couple' of optimization steps inbewteen - evolution has done the same thing for millennia.
A second thing to keep in mind, is that code can be re-used. Programmers already do that (a lot), but usually they try to keep the code readable and make a clean copy for a new purpose. Nature / the genome most of the time doesn't do that and its been re-using and re-purposing pathways on any level for millennia. The reason that arms and legs are built very similar, or that essentially all animals are symmetric is that it's just easier to (re)use the same set of instructions a couple of times with slight alterations than specifically writing everything down.
Finally (as almost always), Randal Monroe explained pretty well, why just knowing the 'source code' of the genome doesn't mean we actually understand how it's doing what it's doing:

This answer's gotten pretty long now and I'm out of time to add sources - if anyone feels motivated to add something feel free to make/propose edits.

Nice answer, +1! Would really like to read some more about the "code reusing" point you made if you can provide some sources :D

@another'Homosapien' one example on the cellular level are second messengers in signalling (esp. Ca2+) - there are only a handfull of different ones, but they are involved in many many different pathways across all celltypes. I'm pretty sure the same goes for (developmental) patterning signals/pathways, but I don't know good examples there.

Ah I did find one: the morphogen sonic hedgehog (yes ...) is involved in developement / shaping of nervous system, limbs, teeth, lungs and still has more functions.

First thing's first: life is an astounding display of emergent properties. I think Nicolai makes that clear in his answer. That is a primary consideration, for how a lot can be achieved with a little. I'd like to make a more philosophical, wishy-washy response to convince you that the genome really isn't all that central to life. Please pardon the metaphors in advance.
The problem we are faced with is that, as Patrick Bateson once quipped,

We can reconstruct a blueprint from a house, but not a recipe from a
  cake.

I'd also like to directly and overtly add that blueprints don't build houses.
In similar vain, you are assuming that the genome is responsible for complexity, when in fact it is only a collection of organized legible macromolecules. Sure, the genome is of paramount importance, and inheritance is crucial for evolution to produce novel attributes, but the kitchen of life depends on much more than just one its recipe books. And it is equally important to understand that genomes are more like recipe books rather than blueprints; you can make blueprints from existing buildings but you cannot make recipes from the cake. Life (and its complexity) is a little bit like cake in this regard.
I'd like to make an extreme case: the fact that the entire system of life requires liquid water means that the complexity of the whole biosphere and organisms is very much tangled with the properties of our sun and planet. This is absolutely a requisite and part-and-parcel of Earth life. The genome does not encode for the position or movement of stars but its genes are dependent on this arrangement. This complexity is, for the sake of simplicity, unrightfully overlooked (for practical and sensible reasons). Carl Sagan put it most succinctly:

If you wish to make an apple pie from scratch, you must first invent
  the universe.


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Caterpillar on milkweed not monarch
Southern California, US and less than 1cm
Please help identify this caterpillar.

Are you sure the plant is milkweed?  The flowers do not look correct.

Welcome to Biology.SE! For identification questions please edit your post to: 1) include the location (e.g. country and region — the more specific the better), and 2) an estimate of the size of the creature. The location and size can be essential clues for identification. ——— If possible clear, closeup photos of the open flowers on the host plant would also be helpful. ——— Please also take the time to go through the [tour] and then the help pages starting with [Ask] questions effectively on this site. Thanks!

I have the same caterpillar on yellow milkweed in San Jose CA and can't figure out what it is either! It doesn't look like traditional photos of tussock moth....

The milkweed looks like Asclepias curassavica, or tropical milkweed. In southern California, it won't die back in the winter, which can throw off the Monarch's normal migration and can cause a harmful parasite to build up. Please be sure to cut it back in the fall and throughout the winter, and consider replacing with a native species.

Ok, firstly:
That plant is not any type of milkweed i know, the flowers are too different.
And secondly:
That's not a caterpillar. It's a hoverfly maggot.
Rather than grubbing about inside decaying roadkill or rotten fruit, hoverfly maggots are predators, actively roaming and searching for prey insects, which in this case would be those little yellow aphids on your plant. After a few weeks of devouring aphids, your little friends will turn into small, skinny flies that greatly resemble wasps(This is so predators leave them alone) and feed on nectar and pollen.

Well done, so +1! There’s even its food source on those leaves. However swamp milkweed and some others have narrow leaves and there appears to be a milky sap on a spot in the first picture right atop a vein. Since the flowers aren’t open yet (the sepals are right), it’s still possiblet that it’s a kind of milkweed.

Hover Fly or Flower Fly larvae.  Feeds on aphids which are most prolific on milkweed plants. They can eat small caterpillars, but aphids are primary. Flower flies feed on nectar and are pollinators. Not annoying house fly category.
Yes, that IS milkweed.  Tropical milkweed brought from Mexico originally and therefore not native to the US.  Considered bad for Monarch butterflies.  Now banned from sale in California in 2022.

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How do parasites "reprogram" brains?
Dicrocoelium dendriticum is a parasite that uses ants as a second intermediate host (which means that ants aren't its primary host/target, but are rather a temporary host to help reach their main/definitive host: sheep).
When ants are infected, this parasite causes them to climb onto the top of grass blades, which increases the chance that sheep will devour the ant along with the grass, helping the parasite reach the sheep.
My question is: how do parasites such as (but not limited to) that described above "reprogram" the minds of the hosts? I know that brains are incredibly complex, so I'm fascinated and curious about how a parasite can change the behavior of its hosts - which I'm assuming is only possible by modifying its brain? If so, how do they do this?

Related Q/A:   can-the-dead-be-brought-back-to-life-by-viruses.

Also related: https://biology.stackexchange.com/questions/23297/what-kind-of-fly-is-this/23298#23298

Not much is known about the mechanisms involved, but they do appear to differ significantly from parasite to parasite. I'll discuss a few different examples here, and try to provide as much information as is currently known about how the parasites are doing it.
There are likely to be many more different examples and mechanisms than these, and researchers may well revise the below hypotheses over time. For this reason, I'm thinking about either splitting this answer into multiple separate answers or changing it into a community wiki.
Example 1 - Toxoplasma gondii and rats as an intermediate host
The Toxoplasma gondii parasite infects multiple hosts during its lifecycle. At one stage, it is hosted by a rodent, which must be eaten by a cat if the parasite is to use the feline's gut in the next stage of its life cycle. Somehow, the parasite causes the rodent (I know that rats are affected, but I don't know if mice or other rodent species are) to behave in a less risk-averse way around cats, making it more likely to be eaten by them.
Exactly how Toxoplasma influences its rodent hosts is unclear. An article in Nature ("Parasite makes mice lose fear of cats permanently") mentions that the parasite creates cysts within the rodent's brain cells, increasing their production of dopamine, which may be one of the causes for the change in behaviour. However, the researchers quoted in the article found that the risk-taking behaviour persisted even without the cysts and dopamine.
Link to that research paper: "Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance".
One theory is that the parasite simultaneously infects the ovaries/testes of the rodent, causing increased testosterone levels in the male and thereby causing it to engage in more risk-taking behaviour. A lot of the literature relevant to this theory is behind paywalls, but as far as I can tell studies have shown that:

Male rats with their testes removed are not affected by the behavioural changes, although I do not know if the orchiectomies were performed before or after infection.
Male rats in general are affected.
Female rats are affected by the behavioural changes, whether or not their ovaries have been removed.

This suggests that the parasite has more than one means of inducing the behavioural changes in the rodent, and that the behavioural changes in female rats have a different cause to the same behavioural changes in males. In the case of the male, it is believed that epigenetics play a part. The increased testosterone levels lead to reduced methylation in genes in a certain area of the brain, and this in turn leads to increased production of the chemical "arginine vasopressin" (AVP). I know nothing about AVP, but the increased levels of it are supposed to cause the behavioural changes, according to this theory.
As I mentioned, the presence of paywalls is giving me some difficulty in studying the relevant research for this particular theory, but a link to one paper is provided in the "Sources" list below.
Another theory is that the parasite infects the white blood cells and causes them to produce excess quantities of a chemical that acts as a neurotransmitter, affecting the brain through the increased levels of said chemical. The research paper is "GABAergic Signaling Is Linked to a Hypermigratory Phenotype in Dendritic Cells Infected by Toxoplasma gondii".
There's also a New Scientist article: "Parasite makes mice fearless by hijacking immune cells")
Example 2 - Ophiocordyceps unilateralis (fungus) and carpenter ants
A recent article in Ars Technica ("Zombifying fungus bypasses the brain to make ants its puppets, study finds") described research into another example, the Ophiocordyceps unilateralis fungus that parasitizes carpenter ants. The researchers had found that the fungal cells in the ant's body effectively disconnected its brain and linked up to act as a replacement brain to move the host's limbs.
Link to the research paper: "Three-dimensional visualization and a deep-learning model reveal complex fungal parasite networks in behaviorally manipulated ants"
(If I understand correctly, the brain's disconnection might be due to damage caused to it by chemicals emitted by the fungus. It may be the case that the original brain and fungal network are both able to move the ant's limbs during the early stages of infection, I'm not sure.)
Even then, one piece at least of the host's altered behaviour wasn't in fact due to this, but due to the fungus destroying a protective membrane on the ants' jaw muscles - leading to the famously strong "death grip" as the infected ant bites a high leaf, dies, and is held in place by the grip of its jaws.

The O. unilateralis fungus extending soma stalks and fruting heads from the bodies of dead ants. Image taken from https://en.wikipedia.org/wiki/File:Ophiocordyceps_unilateralis.png. The image was posted under a Creative Commons Attribution 2.5 Generic license and is credited to David P. Hughes and Maj-Britt Pontoppidan.
The research paper for the jaw membrane is, unfortunately, behind a paywall. If you have access: "Zombie ant death grip due to hypercontracted mandibular muscles"
The "cut off and replace the brain" part of this was also covered by a 2017 article in The Atlantic ("How the Zombie Fungus Takes Over Ants’ Bodies to Control Their Minds").
Example 3 - Dicrocoelium dendriticum and ants
For the actual host/parasite pairing that OP was asking about, not as much is known. One fascinating aspect of this infection is that the ant's behaviour is only changed during the evening/nighttime hours. As day approaches, if the ant has not already been eaten, and if the temperature exceeds a certain threshold, the ant climbs back down to ground level. It rejoins the colony (which does not reject it) and continues to function normally until night falls again, whereupon it climbs back up to the top of the blade of grass.
(In some situations, it may climb up a flower stem and attach itself to a petal.)
A team of researchers used micro-CT scanning to examine the brains of infected ants, publishing their results in a 2018 Nature article ("3D virtual histology at the host/parasite interface: visualisation of the master manipulator, Dicrocoelium dendriticum, in the brain of its ant host")
Most of the parasites are situated in a region of the ant's abdomen known as the "gaster". At this stage in their lifecycle, they are known as "metacercariae". At least one of the parasites, however, will enter a region of the ant's nervous system known as the "suboesophageal ganglion" (SOG). In the brains examined by the researchers, one (and only one) of the parasites in that area would attach its "oral sucker" to the brain tissue of the host ant. This would occur in "the ventral-anteriormost region of the SOG".
The parasites in the gaster are contained within cysts. Some or all of the ones in the brain may not be. The parasite that has attached its oral sucker is not. This one is informally nicknamed "the brain worm".
What is so significant about the SOG region? For one thing:

dendrites of the 10–12 motor neurons that stimulate the fast muscle fibres of the mandibular closure muscles in ants share the same neuropil in the ventral-anteriormost region of the SOG24 – the precise location where non-encysted D. dendriticum metacercariae are located. Thus, by targeting this region of the SOG, D. dendriticum has the potential to directly interfere with ... the action of the mandibles.

Thus we see another mechanism used by a parasite to force its ant host to grip something tightly with its mandibles.
The SOG also has some connection to locomotive activity - presumably getting the ant to climb the blade of grass and/or stopping it from climbing down too soon:

Site-selection and development of non-encysted metacercariae within the SOG can provide a direct pathway for the manipulation of locomotory activity.

And even more...

The SOG is a major part of the nervous system-wide network for neuromodulation in insects, evidenced by the many different neuromodulators expressed in neurons that reside in this region of the brain [25,26,27]. The effects of these neuromodulators ... are diverse and far reaching, from flight modulation, visual dishabituation and olfactory learning to mediation of the fight-or-flight response and the control of aggression ... FMRFamide-like peptide is implicated both as a neurotransmitter and a neuromodulator and affects the nervous system as well as skeletal muscle [25]. Thus, any influence exerted by metacercariae on the activity of neuromodulatory neurons in the SOG could have far reaching consequences for the behaviour of infected ants.

The researchers noted that they did not know if the "brain worm" was in contact with the SOG all the time, or just when the temperature was low enough to induce the changed behaviour. Further research was needed.
Sources:

Ingram WM, Goodrich LM, Robey EA, Eisen MB (2013). Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance. PLoS ONE 8(9): e75246. https://doi.org/10.1371/journal.pone.0075246
Abdulai-Saiku, S., Vyas, A. Loss of predator aversion in female rats after Toxoplasma gondii infection is not dependent on
ovarian steroids. Brain Behav. Immun. (2017), http://dx.doi.org/10.1016/j.bbi.2017.04.005
Fuks JM, Arrighi RBG, Weidner JM, Kumar Mendu S, Jin Z, Wallin RPA, et al. (2012). GABAergic Signaling Is Linked to a Hypermigratory Phenotype in Dendritic Cells Infected by Toxoplasma gondii. PLoS Pathog 8(12): e1003051. https://doi.org/10.1371/journal.ppat.1003051
Fredericksen MA, Zhang Y, Hazen ML, Loreto RG, Mangold CA, Chen DZ and Hughes DP. (2017). Three-dimensional visualization and a deep-learning model reveal complex fungal parasite networks in behaviorally manipulated ants. Proceedings of the National Academy of Sciences Nov 2017, 114 (47) 12590-12595; DOI: 10.1073/pnas.1711673114
Mangold CA, Ishler MJ, Loreto RG, Hazen ML and Hughes DP. (2019). Zombie ant death grip due to hypercontracted mandibular muscles. Journal of Experimental Biology 2019 222: jeb200683 doi: 10.1242/jeb.200683
Martín-Vega D, Garbout A, Ahmed F. et al. 3D virtual histology at the host/parasite interface: visualisation of the master manipulator, Dicrocoelium dendriticum, in the brain of its ant host. Sci Rep 8, 8587 (2018) doi:10.1038/s41598-018-26977-2

Welcome to Biology.SE! Nice answer(+1) and a good job on providing supporting references. However, can you please edit to add references to the original research (rather than just popular science articles) and also include the complete reference information since links can break. Search on Google Scholar and click on the ‟ symbol to get reference information for journal articles. This is a good example of how to format references. Thanks!

@tyersome Thanks - I have now added the references.

The answer to OP's question, while complex and not fully understood, varies significantly depending on the parasite/host combination. Due to the large number of different cases with different mechanisms involved, I would like to either (a) make this answer into a community wiki so that more of these can be added over time, or (b) split it up into multiple separate posted answers. Can any of the moderators/most-experienced users advise me on the best choice here - or should I keep it in its current format?

Regarding my above comment - I may want to add more information over time regarding the different mechanisms of parasite-induced behavioural change, so if this were split into separate answers, I may want to post more answers later on.

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What are the marker enzymes for Nucleus, Ribosomes and cell membrane?
Are there any marker enzymes present for ribosomes, nucleus and cell membrane. For mitochondria there are many, for lysosome it's cathepsin. I read about the marker enzymes of most of the other cellular components, but no information is there on these three.
If no marker enzymes are present then how are ribosomes, nucleus and cell membrane are identified.
I am specifically looking for marker enzymes which can help identify the pellet component after subcellular fractionation.

Why are specifically interested in marker enzymes? And could it be any enzymtically active proteins or are you looking for which activity can easily be measured? Ribosomes are catalytically active (ribo-)enzymes themselves and aren't actual compartments of the cell like all of the other things. The plasma membrane and nucleus are much more heterogeneous than mitochondria or lysosomes so they are usually identified by other markers than enzymes.

You need to describe the experimental procedure in which you need to check for these components. You can see nuclei and membranes under a microscope, and ribosomes are characterized by their components (look them up to see what these are), but I imagine that this may not be what you want. I suspect there is some incorrect premise underlying your question, but without the detail we cannot point it out.


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Photosynthesis production of oxygen
If you are to increase the intensity of light indefinitely, would you expect the production of oxygen to continue to increase?

Welcome to Biology.SE! We encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). Your question as currently written is easily answered by thinking about a moderately extreme case — what would happen to leaf if you directed an industrial laser at it? ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

No. But a simple google search for a graph that shows the relationship between photosynthesis and sunlight (or temperature) would demonstrate this quickly.

No — there are both theoretical limitations and experimentally proven ones.
Chemistry in cells is subject to the same laws as chemistry in general. For photosynthesis to take place, certain molecules (e.g. ADP and NADP+) have to be present to transport the energy harvested to the place where carbohydrates are synthesized from this energy. The transport rate of molecules is limited by the rate of diffusion (see Brownian motion) within a fluid at roughly room temperature (where photosynthesis takes place). This limits the amount of energy that can be processed within a defined volume of plant tissue.
There are further limiting issues. Above certain light intensities, some parts of the plant cell suffer heating and destructive effects, which also limit photosynthesis.
See an abstract on this topic
There are also measured limits. Most plants with leaves exhibit stagnant photosynthesis rates at light with $$600 \frac{μmol}{m^2 \cdot s} $$
or higher.

I made some suggestions that I think improve the wording, but overall a nice answer.  However, I think it would also be good to add references for: 1) the limiting light intensity, and 2) that photosynthesis is limited by the diffusion rate of molecules like ADP/ATP and NADP⁺/NADPH.

I'm going to update that, I'm currently dissatisfied with my answer because it leaves too much unclear about my reasoning and its sources.

Light is one of the factors affecting the light-dependent reactions of photosynthesis. The very low intensity of light will not let the Photosynthesis reaction to occur at its maximum rate and also too much intensity of the light will lead to the bleaching of the chlorophyll. S0, neither very low nor very high intensity is needed for the photosynthesis to occur at its maximum rate.
You can read about this in the article given in the link below:-
http://www.rsc.org/learn-chemistry/content/filerepository/CMP/00/001/068/Rate%20of%20photosynthesis%20limiting%20factors.pdf


text:
What is this toad suffering from? Myiasis or chytridiomycosis?
I found this toad on Aug. 29th at this location: position on osm

I think it is a bufo bufo, approx. 10 cm long. The nostrils seemed to be completely filled with a grey matter and from the activity of the floor of the mouth it apparently tried to breathe againgst this obstruction. It probably had enough oxygen via its skin though.
I tried to remove the obstruction using a blade of grass but this seemed to produce some pain as the toad closed its eyes on contact, so I stopped. The skin looked fairly normal and the toad was able to walk away after a while.
I can think of two causes for this condition.

Batrachochytrium dendrobatidis infestation
Lucilia bufonivora larvae

I could not see properly, if there were any larvae or unhatched eggs inside the nostrils, but as the rest of the skin seemed unharmed I assume the latter.
Is my assumption valid or is there even a third possibility?

It is a female Bufo Bufo and you are right, there are toad fly (Lucilia bufonivora) larvae/eggs inside her nostrills. These flies lay their eggs inside toads' nostrills (specifically on Bufo Bufos) and the larvae start eating them. Sadly this disease ends up by the death of toad. They slowly eat nostrills, then mouth, eyes, and all the head.
Here's a photo of a male bufo bufo, without a head. Someone found it walking around at this situation. https://i.stack.imgur.com/I6twl.jpg

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text:
Speed of electric signal vs chemical diffusion
I'm currently reading the book, "An Introduction to Nervous Systems" by Ralph J. Greenspan.
On page 20, there is a sentence that confused me. It was, "Electrical signaling has the advantage of being able to cover large distances very quickly, much more quickly than chemical diffusion". It is in the context of the primitive signaling mechanism in Paramecium.
My doubt was, isn't the electrical signal caused by the movement of ions? Then how is it any different from chemical diffusion? And again, it's not a electrical signal that travels, but a changing potential, right? Then how does it move at a faster pace than diffusion?

Membrane potential is a directed force, while diffusion is a random walk
Your confusion is entirely justified, as you're correct that both diffusion and depolarization rely on the speed of ion travel. Where they differ is that depolarization is a directed force, occuring only in one direction along the membrane, whereas diffusion is subject to the stochastic walk of ions in water.
When membranes depolarize, the whole membrane begins with a certain amount of "pressure" built up behind it. As the signal propagates, a small area of this pressure is released at a time and triggers the next section to trip. That next section is essentially identical to the previous one, with the same amount of pressure behind it initially. In this way, you can imagine membranes "conserving" the initial concentration, so that the signal strength isn't dependent on the distance from the signal itself.
Diffusion, on the other hand, is stronger initially and decays over distance because of its stochastic nature. It's a probabilistic force, and so depends in general on something like the square root of the distance. If you imagine a thousand ions taking a step forward in one moment, in the next it's equally likely that five hundred take a step backward even as an equal amount moves forward. So the signal degrades over time and distance from the source.
If that was confusing, the following metaphor may help. Depolarization acts like a line of dominos, while diffusion acts like a complex dance. Check out this video of the largest human mattress dominos: the speed they're falling over is pretty constant when they're not turning. Compare that to two dancing humans who are equally likely to move forward and backward, and hopefully you can see that the mattress dominos is the faster way to go, even though each one is theoretically limited by how fast a human could move.

Electrons are >100,000 times lighter than the atom nucleus. For chemical diffusion the entire atom moves, it moves >100,000 times times slower.
Molecular diffusion moves at ~500m/s
Electron signals move at ~50,000,000, m/s
In saline, electrons move at 10% speed of light.
In silver, they move at 95% speed of light.
Crowds of electrons drift very slowly, ~1mm per second. It's called electron "drift". Individuals orbiting and free electrons move at nearly the speed of light.
Conductive materials have free electrons that hop between atoms. If you introduce extra electrons at one end of the conductor, it will push free electrons at the speed of light from one atom to another, while the electron drift stays very slow.
Saltatory conduction travels at 10% the speed of light. Like Dubukay sais, the electrons travel like dominos. The dominos don't travel far/fast but the signal does.
Electrical signals are like a sound pressure wave, where the medium/the atoms stays nearly in the same place, but the electron excess propagates very fast with a wave-front, on a conductive line. only a very small number of electrons move, and they don't move very far at all, i.e. one micron each. The electrons travel like a sound pressure wave. The electrons hardly move but the pressure imbalance moves fast. for chemical diffusion I imagine two colors of paint mixing, atoms travel all through the medium, used by the brain to breach micron distances.


text:
What kind of larvae are these. Lots of them in the basement in the summer, crawling around on the floor and the walls
larvae crawl on basement floor.  Some are also found on the first floor of the house.  Lots of legs--I also thought they became "rolly polys"  but never knew for sure what they were either.

Welcome to Biology.SE! For identification questions please edit your post to: 1) include the location (e.g. country and region — the more specific the better), and 2) an estimate of the size of the creature. The location and size can be essential clues for identification. ——— If possible clear, closeup photos of the creature would be helpful. ——— Thank you for taking the tour — please also take the time to go through the help pages starting with [Ask] questions effectively on this site. Thanks!

"Lots of them in the basement in the summer, crawling around on the floor and the walls" Quick! get some head & shoulders :)

Those are not larvae, but adult millipedes. Myriopoda, Diplopoda. https://en.wikipedia.org/wiki/Millipede
Here is a good link from the U of Minnesota on common arthropods in the basement.
https://extension.umn.edu/insect-relatives/sowbugs-millipedes-and-centipedes


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What is the status of the cfDNA ends?
I am working on a protocol to ligate cfDNA, extracted from blood, into some vector. I have looked into the literature but I cannot find any detail about the status of the ends of the cfDNA. Are they blunt or sticky? What is the enzyme responsible for cutting the genomic DNA into cfDNA?
I know I could blunt it anyway and proceed with a blunt-ligation. However, the amount of cfDNA I have is limited and I would like to avoid purification steps. So, if it tourn out that it is already blunt-ended I would save a step in the process.
Also, protocol aside, I really would like to know more about the cfDNA molecular details and which enzyme is generating it.
Any hint is very appreciated.


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What's this fossil?
I've no experience on the field. The picture below is a gift given to me and I've completely forgotten what was the name of it. I think it was something like "umanite" but I don't know.
It was found on Mt. Vermio in Macedonia in northren Greece.

I'm voting to close this question as off-topic because this is not a question about biology in terms of SE Biology.

What sort of questions does palaeontology apply to?

Unless you are sure that this is a fossil it is not a biology question. Perhaps you can ask in [earthscience.se] first.

I'm pretty sure it's a fossil so I don't see why it should be considered "off-topic" given the designation of "palaeontology" on the site. On Earth-Science "rock identification" is off-topic and questions of biological aspect of palaeontology are off-topic, so I doubt anyone will actually help there either.

it's not alive. It looks like coral fragments. it's blurred. check out a "fossil ID" forum

Respected @user53456 can you kindly add that why you think it is a fossil? Also if it is contains microfossils probably it is impossible to tell from macroscopic view.

Respected @AlwaysConfused I said that I'm "pretty sure" because it was given by a geologist friend back in the university as one. I doubt it was a joke as we were good friends back then. I don't know if it is microfossils as I don't have any experience on the field.

@user53456 I am not confirming your friend did a prank. Microfossils means any microscopic fossils, which include diatom and other protists' shells, pollens, phytoliths (silica crystal found in plants) etc.  and the summed up group's members are not rare either.

@user53456 Rock identification is a valid topic in geology. Anyway, since I am not a member of that community, I can't comment much. Palaeontology is on topic here, in my opinion. Can you post another close-up hi res image of the sample so that the identification is easier? BTW, ammonite sounds like your "umanite" but your sample doesn't look like the former (it looks like a spiral).

Earth scence does allow rock ID questions -- I've asked them! This site does nto handle rock ID, but paleontology would be a valid topic for this site since it is related to biological organisms. However, your post does not have a good picture and I doubt very much anyone in this community will be able to give you an answer. I suggest uploading better photos or asking a paleontologist elsewhere to get a better response.


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Would wasps ever give up on defending their nest against live threat that ignores them?
When I accidentally disturbed a wasps' nest, it was an unpleasant experience. They got everywhere - under my clothes, in my hair etc.
However, in the aftermath - since I'm not allergic to their stings - I observed that apart of some sores on many places on my skin and the racing heart, there's no real damage.
So that made me wonder. If a creature either couldn't feel the stings, or just decided to poke the nest without destroying them regardless of the stinging, would the wasps just give up eventually?
What I mean is, if I just took a stick and poked the entrance ignoring any pain, would they keep stinging until they exhausted themselves to death, or would they just call the defence off and ignore me after a while?

Every wasp acts as an individual so if you disturb a nest, all the wasps that are alarmed will empty their sting on you, that can as many stings as there are wasps. They woudn't call the defense off in any reasonable time. It's not a very rational question. Bears do destroy bee hives, but they have evolved to handle it. I disturbed a hornets nest 10 days ago in a huge black pine tree which i started climbing. Fortunately I didn't get stung by a hornet, even though I had a bike and a track near which is handy for an escape.

@com.prehensible If you keep poking and do not destroy the nest, it must end somehow. Either they exhaust themselves to death or they start to ignore you. That's what I was wondering about.

Yes, but it partly depends on the wasps' perception of "threat". I have had several stings over the years, fortunately one at a time . In E TX the red wasps seem very aggressive , as often as not I do not even know where they came from when I was stung. This year I had 4 stings in 6 days , from small black wasps- something new.. I believe they were "spider wasps" as the stings were very painful and swelling lasted more than 2 days unless treated.  Again , I had no idea I was near them.


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Sharks, alligators and Gould's "random walk" theory
I was thinking about Stephen Jay Gould's view on evolution as pure "random walk" / Drunkard's Walk, increasing or decreasing complexity in basically random fashion, just limited by death if an organism becomes too simple and so increasing complexity without meaning that it somehow confers survival / fitness advantage.
Now, I've read elsewhere that at least some of the shark species (subspecies?) have existed in about unchanged forms for at least 100 million years (correct me if that's wrong) and alligators for 37 million years. 100M years or 37M years is pretty long even for evolution, so wouldn't it create pretty high chance that such long-running species would die out and/or evolve into species even more complex (per Gould's claim of complexity systematically increasing for purely random reasons)? Why would then what seems like about optimum fitness for particular environment persist so long?
Note: obviously I'm not a biologist or even student of biology, evolutionary biology is just my occasional interest. Apologies if I made basic mistakes in premises to this question.

You may be making a very common mistake in reasoning about probabilities. Yes, it is very unlikely that a particular species, picked at random,  would persist largely unchanged for 37 million years, but at the same time it might be almost certain that some species would follow that course. The error is that you didn't pick a species at random, you picked it precisely because it showed that high degree of conservation. It's equivalent to accusing the winner of the lottery of cheating, because winning is so unlikely. Yet the lottery is designed so that somebody wins almost every time.

You're also ignoring the optimization factor.  Living in water puts some severe constraints on creatures, particularly on their shapes, due to hydrodynamics.  Sharks in general have converged around a local optimum - and ichthyosaurs, dolphins, and tuna have converged around the same one.  It takes a large evolutionary jump to get out of that optimum.  And since what we see of fossils is mostly their shape, we don't see much change in general "sharkness".

@CharlesE.Grant Well... it's a different lottery winner almost every time, isn't it? Let's say we calculate the probability of alligators staying almost exactly the same over 37M years using binomial probability formula.

@CharlesE.Grant: Calculation: p = 0.999999 (probability that gator species will stay the same over all generations), q is the usual complement, n = r = 37^6. Since n = r, Newton's binomial in the formula = 1, q^(n-r) = q^0 = 1 and so the whole formula boils down to p^r, presuming simplistically that 1 gator generation takes 1 year. Hence, the value is 0.999999^37000000. This probability is so low that my Gnome calculator doesn't even display the actual value, rounding it down to zero.

@jamesqf: "You're also ignoring the optimization factor. Living in water puts some severe constraints on creatures, particularly on their shapes, due to hydrodynamics. Sharks in general have converged around a local optimum" - well... that's my point. Had constant selection pressure not kept shark's complexity pretty much the way it is, sharks would have evolved into something else, by Gould's argument evolution increasing complexity "mindlessly" via random walk, which is not happening.

@CharlesE.Grant: although I think what you may have meant: in a large number of random trials some individual species will be winning systematically more than others due to sheer chance, kind of like if you see stock market as a random walk, some traders will win more than others due to sheer chance and not because they're better. Still, "more than others" does not meand scoring every time better than others. Probability for scoring r successes in n trials with n = r is like I calculated for everyone, which means that basically no trader  or species will "succeed" every time.

@CharlesE.Grant: oops, there's a typo in my initial reply: I meant p = 0.999999 is probability that the gator species will stay the same over one generation, not all generations, obviously.

Assuming there's an upper bound and a lower bound to complexity, e.g. it hopefully can't get simpler, physically, than an atom/quark and there are I'm sure, physical limitations to complexity (one is Galileo's square cube law). If evolution is truly random, we have a yin-yang effect. After evolution (whether complexification or simplification) hits the boundary walls, the random walk will reverse direction and move towards the other limit. However, in the simple simulations I've conducted, sometimes the random walk stays steady at max/min i.e. plateaus at the upper/lower bound, for some time, and then, "having nowhere else to go", proceeds in the opposite direction, towards the other limit.
In the diagram below of a 1D random walk, look at the region circled in purple. A tendency, albeit brief, to remain at minimum.


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What is a Singleton Variant
I'm reading a paper that on a population genetics study where they sequence a number of genomes. The study states that 101 Singleton Variants per individual where found. What does Singleton mean?

A singleton in mathematics is a set with one element.
They are likely referring to variants found in only one individual in their pool. It's possible there are other uses of the word singleton but given the context I think it is most likely.


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Does the 1:1 sex ratio at birth apply to every human pregnancy or is it a statistical average?
Are there genetic factors that biase the sex ratio of offsprings for each person but average to 1:1 for the entire human population, or does the 1:1 ratio apply to every single fertile person?

The ratio is not 1:1: https://biology.stackexchange.com/questions/27582/why-do-we-have-more-male-infants-born

@kmm The question still stands -- is the ratio a statistical average or applicable to individuals?

The ratio you are referring to is indeed computed aggregating multiple observations and thus it is a "statistical average".
Any individual (or couple, in this case) can have a specific ratio that differs from the average one. Many factors may affect sex ratio, among which sperm/egg viability, chromosomal aberrations, and hormones misbalance are the ones usually affecting the fertility of a couple and they can also bias the sex ratio.
Many other factors can play a role.
Different populations have slightly different sex-ratio and even smoking can skew the sex ratio!

The question is not very well asked but I suppose the OP does not ask whether any given couple can have more offspring of one sex than of the other but rather whether there is genetic variance in the sex-ratio.

@Remi.b I have interpreted the question differently. I will wait for the OP to comment to this answer or to clarify the question. If needed, I will adjust my answer.


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Viral RNA to DNA
I have a question concerning reverse transcriptase.
Why is it that when the viral rna is converted to viral dna( as in the case for hiv), the virus develops resistance to medicine?
Under what circumstances does reverse transcriptase causes a viral mutation?

Welcome to Biology.SE! We encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). For example, the top hit I found searching with "mutation-rate reverse-transcription" was: https://www.ncbi.nlm.nih.gov/pubmed/12456349 ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

Via: https://en.wikipedia.org/wiki/Reverse_transcriptase#Replication_fidelity

There are three different replication systems during the life cycle of a retrovirus. First of all, the reverse transcriptase synthesizes viral DNA from viral RNA, and then from newly made complementary DNA strand. The second replication process occurs when host cellular DNA polymerase replicates the integrated viral DNA. Lastly, RNA polymerase II transcribes the proviral DNA into RNA, which will be packed into virions. Therefore, mutation can occur during one or all of these replication steps.[17]
Reverse transcriptase has a high error rate when transcribing RNA into DNA since, unlike most other DNA polymerases, it has no proofreading ability. This high error rate allows mutations to accumulate at an accelerated rate relative to proofread forms of replication. The commercially available reverse transcriptases produced by Promega are quoted by their manuals as having error rates in the range of 1 in 17,000 bases for AMV and 1 in 30,000 bases for M-MLV.[18]  (Emphasis added.)

Polymerases are proteins (enzymes) that make copies of genetic material: DNA or RNA. https://en.m.wikipedia.org/wiki/Polymerase
These enzymes have different fidelity or error rates. This means that different polymerases can make fewer or more mistakes when copying genetic information.
To accommodate errors, DNA polymerases have proofreading mechanisms that go back and fix errors. Most of the time, this works as expected.  https://en.m.wikipedia.org/wiki/Proofreading_(biology)
However, the reverse transcriptase that copies RNA into DNA does not do any proofreading, so there will be various mutations in some fraction of copies, depending on the transcriptase's fidelity rate. https://en.m.wikipedia.org/wiki/Reverse_transcriptase
For viruses, it is a pure numbers game. All they are programmed to do is make copies of themselves, and as many copies as possible, when they are in infectious, non-dormant state. https://en.wikipedia.org/wiki/Lysogenic_cycle and https://en.wikipedia.org/wiki/Lytic_cycle
Most mutations will be deleterious and the virus won't infect, integrate, and replicate successfully. A random mutation will often break a needed protein involved in the viral reproductive cycle.
Some mutations are "neutral" or "silent" and won't change how the virus copies itself. Consider that the genetic code is redundant — substitute a base here or there and you can still get the same amino acid sequence. https://en.wikipedia.org/wiki/Silent_mutation
But if you have enough virus particles copying themselves, all you need are mutations in the parts of the virus genome that allow it to keep replicating and also change the proteins it makes, just enough to evade the host's immune system.
If a mutated virus can still replicate and also change the proteins it gets the infected cell to make on its behalf, it can be more successful at copying itself. Immune cells will have to "relearn" whatever changes were made in order to trigger the usual immune response and fight back.
In the case of HIV, it also attacks the immune system directly, which is another complication.
Medications try to interfere with the different ways in which HIV works to infect immune cells and to make copies of themselves.
For example, one class of medication tries to "compete" with the part of HIV that binds to the surface of T cells. It's like a night club, where the bouncers at the doors are more likely to keep HIV from getting into the cell/club and partying.
Other classes of medication interfere with a protein called integrase that HIV makes to integrate its viral DNA into the host DNA. Integration of the HIV DNA into the host cell's DNA is a critical step for infection, so that's one way to target the virus. https://en.wikipedia.org/wiki/Integrase
Still other drugs try to inhibit the reverse transcriptase that turns HIV RNA into DNA. If the virus RNA is inhibited from being made into DNA, then that can help keep further infection in check. PrEP is a combination of two drugs (tenofovir and emtricitabine) which are RT inhibitors. https://www.cdc.gov/hiv/basics/prep.html
An overview of some of these medications is available here: https://www.webmd.com/hiv-aids/aids-hiv-medication
These medications all try to target the proteins involved in how HIV infects and replicates inside immune cells.
In turn, reverse transcriptase is sloppy enough in turning HIV RNA into DNA that it can get lucky and mutate enough to make one or another medication less effective.
Treatments are sometimes put into so-called "cocktails" of multiple drugs. A multi-drug regimen that attacks the virus by different means will give HIV a harder time in getting lucky enough to mutate in ways that it can get past a multi-pronged attack in those who are HIV+. Another good summary of such medications — many of which target reverse transcriptase activity — is available here: http://www.aidsinfonet.org/fact_sheets/view/403


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What forms this pad on the side of the face?
I've been trying to figure out this for the best portion of this morning, but what structures are responsible for the pad highlighted in red? (sorry for low quality of picture, was just watching the show at the time)

It's from my understanding that the zygomatic (in green) runs to the edge of the ear in a relative straight line and most muscles have their origins or insertions bellow it. I know there are some fat pads (such as the nasolabial fold in purple) on top of everything on the face, but are these all fat pads that just allign? I've seen this pad on both man and women often, although it seems more proeminent in women.

That padding is apparently from a prominent zygomatic arch also known as high chickbones (pictures).
The bones between the eye, nose and ear are: the zygomatic bone below and behind the eye, the zygomatic process of the frontal bone above/behind the eye and the zygomatic process of the temporal bone, which extends toward the ear canal. It makes sense that when the zygomatic bone is more prominent, the zygomatic processes of the connecting bones will be also more prominent and appear as high cheeks.

Image source: Wikimedia, CC license
Here's the photo of Abraham Lincoln from the Wikipedia's article about zygomatic bones:

A Youtube video The Zygomatic Bones and Ogee Curve

I can see the presence of the zygomatic bone on the front of the face, and consequentially on its profile and shape under the eyes. What I am refering to is the continuation of the form on the side of the face, behind and above the lateral eye line and where the zygomatic and zygomatic process end, all the way to above the ear.

@omiyage, I changed the answer and the pictures. I believe, the padding is due to prominent zygomatic arch, so due to the bones.


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Got stung by this flying bug in Death Valley and Arches, what is it?

We camped in Death Valley and these guys were attracted to light and ended up stinging us. Didn't hurt as bad as a bee Sting. Any ideas what they are? Couldn't find them doing a Google search or image search.

Please provide an approximate size. Also, the more information/photos you provide, the better chance of getting the correct answer. Please [edit] your post with more detail. Thanks

A photo with the wing venation in focus should be among your additions; from what is here, we can say Hymenoptera (bees, wasps, ants, et cetera), but not an ant (the antennae don't have a distinct angle between the first segment and the second).


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Why do some texts say that noncompetitive antagonist dose no change in ED50 of agonist in Dose-respond curve?
Competitive antagonists increase the ED50 while the Emax remains the same. Non-competitive antagonists do not change the ED50 while decreases the Emax.
I wonder how does this happen as Non-competitive has no effect on ED50.


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How many recombinations occur in an average human chromosome?
And is it a different number depending on which chromosome we choose (disregarding the change of this probability due to the differential size of the chromosomes)?

Welcome to the site!  Unfortunately, this is really too broad... It will definitely depend which chromosome you chooose, and in any case, recombination can occur during mitosis or meiosis... You'll really need to narrow down your question.  Thanks!

I was asking about recombination during meiosis, the recombination that homologous chromosomes undergo to produce gametes. I had no idea recombination took place during mitosis, unless you mean something totally different to meiotic recombination that happens to have the same name. So the question would remain like this: how many sites of recombination are there in, say, chromosome 1? (Although I would also like to know how much that number varies along every chromosome).


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Do animals like Seals feel cold on their skin?
Whenever there is a documentary about animals and you get to the colder regions, you will hear about Seals and their layer of blubber keeping them warm.
But the skin is on top of the blubber, in direct contact with the cold water (and air). Do they feel the cold outside the way a human would?

We don't really sense temperature on our skin, we sense heat exchange (see Do humans perceive temperature or heat-flux?. It is for this reason that a 10˚C piece of wooden spatula feels very different than a 10˚C copper pan.

Humans (and other animals) do not feel temperature; when we “feel cold” we actually sense that our body starts to lose heat (we feel the heat transfer). Pinnipeds, notably phocid seals (True seals or earless seals), restrict heat transfer to the environment by reducing skin temperature. To do so, phocids have a thick layer of subcutaneous blubber (or hypodermal adipose tissue) with a low thermal conductivity, which significantly reduces heat transfer via conduction (insulating the skin surface from the body core). On contrary, flippers are the areas of the body with little blubber. Interestingly, in phocids, flipper skin tends to be the least emissive region during cold weather (Kharmas et al. 2012), which could be explained by the presence of counter-current heat exchangers (found in the flippers of pinnipeds). Counter-current heat exchangers (another thermoregulatory strategy) are present in peripheral body parts and help retain heat in the core body by rewarming cold venous blood returning from the periphery as it passes in proximity to outgoing, warm arterial blood. To summary, phocids limit heat transfer with a blubber layer and control heat transfer by using blood flow (see Favilla and Costa, 2020 for a review about Thermoregulatory adaptations in marine mammals).

This doesn't really answer the question. I know heat transfer is limited, but the skin on the outside of the animal is in direct contact with the cold. As far as my knowledge goes at least. Does the heat retained inside the animal warm it enough to not feel the cold from the outside?

FYI: Phocid seals have short hair. Their skin has nerve cells sensitive to temperature (similar to other mammals), so yes they might have the ability to sense temperature. About your question can they "feel the cold", do you mean like experimenting discomfort? It's a difficult question. Those animals are adapted for cold climates.


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The Collagen Triple Helix
In the amino acid sequence X-Hyp-Gly (where X can be any amino acid) of the triple helix can the Hyp residue be both hydroxyproline and hydroxylysine? In our textbook it says that the Hyp residue is hydroxyproline but "hydroxylysine also occurs in the collagen".
Thank you!

Welcome to SE Biology. We can answer this question for you, but you will learn more by thinking about the structure of the amino acids and of collagen, and WHY every third residue might be hydroxyproline, and whether the structure of lysine would allow it to perform a similar function. (This is also what we expect of people who post questions.) Look at one of the online texts at NCBI bookshelf — Lodish, and perhaps this article. Come back and tell us what you found.


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How do we know if a neuron is inhibitory or excitatory?
The textbook examples for an excitatory neurotransmitter is Glutamate, and for an inhibitory neurotransmitter it is GABA.
In my naive understanding, a neuron was inhibitory or excitatory depending on the neurotransmitter it releases onto its postsynaptic partners.
According to this thread, however, a neurotransmitter is not per se excitatory or inhibitory, but this property depends on the postsynaptic receptor it is acting on.
Now this property seems independent of the presynaptic cell - hence, how can we classify the presynaptic cell of being either inhibitory or excitatory (when that is a property of the postsynaptic receptors, which can be either)?
Besides, given that we a huge number of neurons and their connections in each $mm^3$, how can we be sure that the presynaptic's cells action are not mediated by other cells, and the observed inhibition/excitation is not rather a network effect?

In my naive understanding, a neuron was inhibitory or excitatory depending on the neurotransmitter it releases onto its postsynaptic partners.

This is mostly correct. What remains a question is what makes a given neurotransmitter inhibitory or excitatory. To some extent, that depends on the post-synaptic receptors, but also depends on other conditions: one case mentioned in the linked Q&A that I'll repeat is that GABA is actually excitatory at some times, including during development (and the same thing can happen in certain causes of epilepsy). In that case, the reason is because GABA-A receptors are chloride channels, so the reversal potential for chloride is what matters. If the reversal potential for chloride is more hyperpolarized than threshold, GABA-A is an inhibitory receptor; if the reversal potential for chloride is more depolarized than threshold, GABA-A is an excitatory receptor. Chloride ion concentrations are different during certain stages of development so the role of GABA changes (in development it seems like it is important for development of eventually inhibitory circuitry).

I digress a bit, but I think you've really already encountered all you need to know: labels like "excitatory" and "inhibitory" for a neurotransmitter itself are generalizations that satisfy human preferences for heuristics. It's convenient to talk about GABA as an inhibitory neurotransmitter, because in most cases the major systemic effect of GABA is inhibition. Same with glutamate in the direction of excitation.
Most of the inhibition caused by glutamate is the presynaptic inhibition type discussed in a previous Q&A; that is, it is suppressing the release of glutamate itself. In that sense, glutamatergic inhibition is only as effective as glutamatergic excitation is: the net effect of glutamate will always be excitatory in that system.
Therefore, it is straightforward to consider GABAergic and glutamatergic cells inhibitory and excitatory, respectively.

how can we be sure that the presynaptic's cells action are not mediated by other cells, and the observed inhibition/excitation is not rather a network effect?

The principle way is by pairwise recordings: you record from the presynaptic and postsynaptic cell at the same time, activate the presynaptic cell, and measure the voltage in the postsynaptic cell. These sorts of pairwise recordings are a common tool in neuroscience.

Cancedda, L., Fiumelli, H., Chen, K., & Poo, M. M. (2007). Excitatory GABA action is essential for morphological maturation of cortical neurons in vivo. Journal of Neuroscience, 27(19), 5224-5235.
Owens, D. F., Boyce, L. H., Davis, M. B., & Kriegstein, A. R. (1996). Excitatory GABA responses in embryonic and neonatal cortical slices demonstrated by gramicidin perforated-patch recordings and calcium imaging. Journal of Neuroscience, 16(20), 6414-6423.
Thomson, A. M., & Deuchars, J. (1997). Synaptic interactions in neocortical local circuits: dual intracellular recordings in vitro. Cerebral cortex (New York, NY: 1991), 7(6), 510-522.

"The principle way is by pairwise recordings: you record from the presynaptic and postsynaptic cell at the same time, activate the presynaptic cell, and measure the voltage in the postsynaptic cell." --> But this is still a correlation analysis. Say you activate cell A and record A and B, how can you exclude A acting on C,D,E...with all kinds of non-trivial interactions then leading to changes in B? Then while A would still be relevant for B, the excitation/inhibition might arise from more complex mechanisms.

@Pugl No, it's not a correlation analysis: you stimulate and measure the response. A correlation analysis would just measure activity in both and relate the (spontaneous) spiking times to the voltage. You can base conclusions on latency, use brain slice recordings where spontaneous activity is very low (such that only the cell you are activating is likely to be firing, and especially only that cell is firing time locked to every stimulation trial), in some cases record directly from dendrites and even axons in special synapses.

You can use pharmacology to test which transmitters and receptors are involved, directly puff neurotransmitters onto the post synaptic cell and see the same results, you can use imaging to monitor voltage or calcium in real time, you can activate presynaptic terminals with calcium uncaging. Basically decades and decades of neuroscience research.


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Can we "learn" reflexes?
Can we force our bodies to react to situations faster than our brain can think about them?
Some reflexes I can think of off the top of my head:

knee jerk reflex
retracting hand when touching a hot pan

Not sure if these are the same type of reflex, the second might be using the brain.
Can we instil into ourselves similarly fast reaction times to other stimuli?

Certainly, though "reflex" is probably not the correct technical term.  Practice fencing, for instance, or other martial arts, and you'll experience this for yourself.  Or even riding a bike.

Often called "muscle memory" in some sports or activities - using knives fast like chefs do...

@Solar Mike: Likewise playing keyboard or plucked musical instruments, or FTM typing.

@jamesqf but is muscle memory actually a reflex like the knee-jerk is, doesn't the nerve signal have to travel all the way to the brain first


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Is there any (practical) way to control a rodent population without predators?
It seems that New York has tried a number of ways to reduce their rat population, recently with fall traps. Unless they can kill all of the rats at once, it seems that this will just free up resources for the surviving rats to use. A feral cat population (which would increase in response to its food resource, i.e., the rats) seems to be the best way to control this. From an ecological perspective, are there alternatives to controlling a population of rodents, apart from using predators?

While your question is interesting, it is asking for opinions. Moreover, answer to this question would not be straightforward and require a lot of details and explanations and thus making it unsuitable for the stackexchange Q&A format. Perhaps you can search for some reviews on this topic.

There has been talk of controlling mosquito populations with CRISPR and gene drives. You can read about it from Nature (https://www.nature.com/articles/d41586-019-02087-5). In the future this may be possible for rodents.


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Could ions inside lungs produce hydroxyl?
I am not proficient in either biology or chemistry. However, I have a question which I can't find answer to. It seems to belong somewhere between chemistry and biology. I apologize for any errors and inconsistencies in this post.
There is a page (https://allergytech.com/sharp_plasmacluster_ion.htm) which describes a process. During this process, positive and negative ions are released to the air. They are called clusters.

The clusters seek out and surround harmful airborne substances such as
  fungi, viruses, microbes, bacteria, plant and mold spores, dust mite
  debris, etc. At this point, a chemical reaction occurs, and the
  collision of hydrogen with oxygen ions creates groups of highly
  reactive OH radicals, called hydroxyl - Nature’s form of a Detergent.

A hydroxyl radical is very unstable. To stabilize itself, it robs the
  hydrogen from any harmful airborne particles it encounters. Doing so,
  the hydroxyl radical damages the harmful micro organisms and
  deactivates them.

Below is my question.
Suppose that a human breaths in those clusters as soon as they are released to the air. Is there a possibility that inside lungs, they will encounter something that will trigger similar reaction, and in effect hydroxyl will be created, too?

I’m sorry but questions on SE Biology should be comprehensible in themselves, without the requirement to go to some third party website which may be booby-trapped or disappear tomorrow. You need to post the images at the very least.  From what you write your understanding of chemistry seems deficient. You need to sort that out too, because at the moment what you write makes no chemical sense.

Thank you. I’ve looked at the page. It seems to be an ad for snake oil.

I don't know, maybe it's an ad. The technology is described in other places like here and here. But I can't find explanation what happens to the lungs when you inhale those ions, whether they could break lung cells like they break airborne particles.


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Vasoconstriction and blood flow
The resistance in a blood vessel is equal to the pressure difference divided by the blood flow. Let us now say that a sympathomimetic causes vasoconstriction which increases the resistance. Does this primarily increase the pressure in the blood vessel? Does it primarily reduce the blood flow in the blood vessel?
In context, the filtration fraction of the kidneys is the GFR divided by the plasma blood flow through the afferent arteriole. The sympathomimetic would in general increase the filtration fraction by reducing blood flow. However, the GFR is also dependent on hydrostatic pressure which may increase if there is a rise in resistance. Therefore, shouldn't the filtration fraction change minimally due to the rise in GFR counteracting the fall in blood flow?


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can auditory/ocular reflexes exist?
In the same way the knee-jerk reflex is a thing (I think the nerve signal doesn't go through the brain?), can stimuli received by the eyes or ears trigger "instantaneous" (faster than the brain can process it) responses?

The wikipedia article on reflexes has a section listing "Reflexes involving cranial nerves" that seems relevant to your question ...

Short answer would be yes. There are very simple examples such as responses to sudden bright lights controlled in the Trigeminal nerve bundle to constrict pupils. Visual reflexes are interesting because it can frequently involve a neuron crossover in the nerve bundle. This would be an inappropriate reflex due to a stimuli. The most common being suddenly being exposed to a bright light causing you to sneeze like pepper was thrown in your face. Also interestingly this is an autosomal dominant trait so one of your parents will have to have the same response for you to inherite it.
Photic sneeze response

As for audition you have the stapedius reflex, or auditory reflex, that contracts muscles of the middle ear to reduce the transmission of loud noises to the cochlea.


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Were there any vertebrates with 6 or more limbs?
My question is actually a bit more broad than what's in the title, but I don't know how to put it succinctly.  When I was trying to find the answer to that question, I found that all known terrestrial vertebrates are ultimately descended from a species of lobe-finned fish that had 2 sets of bilaterally symmetric fins (which excludes the dorsal and ventral fins), which were the basis for the limbs of its tetrapodal descendants.
The best way I can think of to phrase the question is: Does paleontology has any evidence of a vertebrate that had 3 (or more) sets of bilaterally symmetric limbs or lobe-based fins?  I'd like the focus to stay away from ray-finned fish, even though they're vertebrates and related.
This is not the common question, which is whether there is or can be a mammal/reptile species with more than four limbs.  The essence of that question's answer is that mammals and reptiles both evolved from a common ancestor species that were tetrapods, and that it's extremely difficult to change the genetic floor plan in the necessary way without causing fatal problems (along with other evolutionary issues).  By and large, this common question is so common that it chokes out the type of question that I have, making my amateur attempts at further research difficult to impossible.

Related: Why don't mammals have more than 4 limbs?

I've not read it but this SE question Why don't mammals have more than 4 limbs?
though not a duplicate (it asks about mammals not all vertebrates) may have some elements in its answers pertinent to your question.
And the question Why are there no vertebrates with more than four limbs? has been asked in Quora where it has 7 answers you may find useful.
Also this discussion thread Why can insects have 6+ limbs, but mammals only have 4? in reddit.

Does paleontology has any evidence of a vertebrate that had 3 (or more) sets of bilaterally symmetric limbs or lobe-based fins?

You sent me far down the rabbit hole with this one, for reasons that escape me my instant response was 'yes the Coelacanth' but as you correctly point out that has only 4 paired fins.
As seen from The origin of tetrapods our limbs came from fins, Coelacanth is a good example of the likely early beginnings of Tetrapod limbs, they occasionally use them to 'walk' on the seabed.
The image provided in this National Geographic article Coelacanth Rediscovered gives a much clearer picture of it's 'limb' structures.

Latimeria chalumnae, the coelacanth (SEE-lee-uh-kanth), thought extinct until a biologist identified one off the coast of South Africa in 1939.
I've trawled Google for early chordates looking for examples of more than two pairs of fins & haven't been able to find any, it seems the earliest paired fins appeared in (or shortly before) Ostracoderms & from there continued in an unbroken line to the tetrapods & our limbs.
Paired fins don't appear to have developed in chordates before then or to have ever developed into more than two pairs.
So to the best of my knowledge it appears that the answer to your question is no.
Other links.
Yunnanozoon
Myllokunmingia
Haikouichthys
Evolution of fish

Far later edit: I "might" have found one?
Came across this article on Polymelia which says "Mesacanthus developed a third pair of paired fins" // & this article on Mesacanthus I then found says besides the normal paired pectoral & paired pelvic fins it had "a pair of prepelvic spines".

"there have never been any land vertebrates with anything other than four limbs." - snakes. If there are any vestiges of limbs on their skeletons, I haven't been able to spot them. And there certainly isn't anything on the outside.

@JohnDvorak : Snakes were just 4 limbed lizards b4 losing the last vestiges of their limbs, they are for the purpose of this question four limbed animals I feel, you can even prod the embryos hormonally to grow limbs if you want, it's all still in their DNA they just don't express the genes, but point noted :)

While the coelacanth has 6 fins (along with many related extinct species), only 2 sets have bilateral symmetry, the remaining 2 fins are unpaired dorsal and ventral fins.  The information in the links has been interesting, though I'm still combing through it.

I would shy away from pointing people toward Quora or reddit since the answers on both sites are often not factual, opinion, and lack adequate peer review for accuracy. Referencing such sources of information is, in my opinion, reckless and very potentially misleading.

@theforestecologist I'd more or less agree with you, particularly about reddit, but they do occasionally provide links (or even just technical words I hadn't thought of useful for a search) & can make a useful jumping off point as a result.

@Pelinore that may be true, but I think relegating such sources to minor footnotes would be more appropriate than citing them in such a front-and-center fashion as in your post. (e.g., something like "you can find similar posts on less-reputable sites like Quora or reddit to use as further jumping off points"). Again, I think information on both of these sites are notoriously dubious, so I would personally suggest/request you help to slow the spread of misinformation by not promoting those sites as prominent parts of your answers here. We're trying to maintain higher standards here at SE :).


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Is there vascular supply to cartilage
According to Gray's anatomy, cartilage is avascular but in a recent class, my teacher told me that there is vascular supply but it is confined to upper surface only. So, I'm confused that who is correct.

How do you define "upper"? My suspicion, however, is that there is no conflict: avascular tissue can still be supported by a blood supply, avascular just means there are no vessels in the tissue itself. It's probably best to just clarify this with your teacher.

I think that by upper, he meant surface region.

Then I think most likely there is no conflict and just misunderstanding. A tissue that is supplied only from its surface is equivalent to one that is avascular.

Thank you for the clarification.

This depends on what kind of cartilage you are examining and where it is located. Cartilage is not all the same depending on where it is located and it's intended purpose. Cartilage also generally exists as a continuum with the bone that it is attached to where you will see transitional changes from bone tissue to cartilage without specific delineation. Depending on the cartilage location and its function it may of may not be vascular. Hyaline cartilage existing closest to synovial joint spaces is pretty much entirely avascular. This has some advantages and disadvantages. Damage to cartilage is very difficult for you body to repair for myriad reasons one being avascularity, but also the avascularity allows for you to transplant live cartilage to any person regardless of what tissue type the donor or recipient is.


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Is recapitulation theory correct?
Most school books still say that recapitulation is an evidence of evolution but as far as I know it has been proved wrong so why is it being still taught? Has it got any sort of relevance?

It is not correct and is outdated. However, it is a compelling hypothesis and was formulated based on interesting pieces of evidence. It has been discussed on this SE before, please use the search function. See e.g. this answer of mine, and the rest of the thread or this excellent article from 30 odd years ago.

Welcome to SE Biology. Your question has a couple of problems. First, you should explain breifly what recapitulation is. I don't know. Then you should cite an actual modern text book that still presents it. Then you should explain the basis that it is thought to be incorrect so that your question is about a clear and specific biological idea, that can be answered objectively. Don't ask questions in terms of "why it is being taught" — an answer may well be out of the realms of biology. Ask, instead, whether a scientific argument against the idea is correct.


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Is variation a result of Evolution?
We know that the DNA copying mechanism that replicates DNA during cellular division is not 100% accurate and the resultant errors are the source of variation in the members of a population.
At the same time, we are also aware of the benefits of variation - how it is useful in ensuring the survival of a species over time and leading to evolution.

I would however like to know if 100% accurate DNA replication is possible (even if hypothetically) - because in my opinion, organisms can surely survive (atleast individually) without variation or evolution.
If it is so, is it possible that organisms with 100% accurate DNA replication did exist, but eventually their populations died out (due to natural selection) and we were left only with organisms that showed variation?

Putting in simpler terms, it is possible that evolution itself is the cause of variation that now causes further evolution?

Related: https://biology.stackexchange.com/questions/378/has-there-been-any-observation-of-species-adapting-the-evolution-process

For your question about whether 100% accurate replication is possible, think carefully about multicellular organisms. Any evolutionary benefit to mutation would have to be in the germ cells. For non-germ cells, you (in most cases) want as little variation as possible since that variation will never been heritable.

There are many kinds of DNA replication errors that lead to mutations some of them could be 100% error free some are inherently not possible.

Hypothetical questions of this sort — in this case flying a kite rather than posing a question that can be answered objectively — are off topic here.

@David I would like you to elaborate.

@Cell Thanks for the response. I am interested in knowing more about the same.

@BryanKrause I totally agree. How does that but explain my doubt.

@MrigankPawagi I'm trying to steer you towards a more answerable, non-hypothetical question. If 100% error free replication is possible, we'd have something like it in somatic cells. If allowing errors in germ cells is beneficial, we'd expect higher error rates in germ cells.

If you go to the Tour, you will read: "Focus on questions about an actual problem you have faced. Include details about what you have tried and exactly what you are trying to do. Ask about... general questions about biological concepts, questions about the biological mechanisms behind medical conditions, questions about techniques in a biological or biochemical laboratory". And "Not all questions work well in our format. Avoid questions that are primarily opinion-based, or that are likely to generate discussion rather than answers."

Another piece of advice in regard to posting questions is to do some research on the topic first. I suggest you read about Errors in Replication in this Scitable article. Here you will read "Fortunately, cells have evolved highly sophisticated means of fixing most, but not all, of those mistakes." Think about it.

error free replication would only be helpful if a species was perfectly adapted for its environment AND its environment never changed. because environments change constantly it would never be an advantage.

You're asking if cells arose with 100% replication accuracy and if lower accuracy was selected for under a feedback loop. Maybe there was a sweet spot for DNA replication accuracy in terms of efficiency, but it's highly unlikely that our ancestor cells had 100% fidelity in DNA replication because if we look at yeast for example, there are many genes dedicated to different types of post-replication repair including mismatch repair, base excision repair, and translesion synthesis. All of these can lead to mutations if they aren't working properly and some (translesion synthesis) inherently generate mutations. It doesn't seem consistent for a cell to develop all of these sophisticated post-replication repair systems to protect itself from DNA damage and then to give some more leeway to DNA replication because it was just too accurate.
Also there are papers like this that talk about how E. coli have increase mutation rates under stress. But if your hypothesis was true, then E. coli would ideally have 100% replication fidelity under normal conditions and lower it when stressed, or they would just have a higher baseline mutation frequency all the time. But, neither of these is observed. What makes the most sense when all this information is put together is that cells try to have as high DNA replication fidelity as possible under ideal conditions.
As per your other question, maybe it's possible to have a 100% accurate DNA polymerase  NEB engineers high fidelity polymerases for lab use maybe someday it can reach 0 errors. But there are other sources of mutations like the spontaneous deamination of cytosine that can generate mutations during replication, but that depends on the chemical properties of cytosine so it's not really fixable unless you use different nucleobases.
Reference:
Mutation as a Stress Response and the Regulation of Evolvability. (2012)
By: Rodrigo S. Galhardo, P. J. Hastings, and Susan M. Rosenberg

Great answer. I have read about E. Coli and I am totally convinced with your point about the post-replication repair in yeast.

There is previous research for that field of macroevolution.... Horse shoe crabs change slowly and tropical fish change fast.
You are right, it's not just random variation, it's fine tuned by DNA transcription processes which are too developed to be random, so the complexity of the processes leads scientists to think "WTF" regarding epigenetics, transgenerational phenotypic plasticity, paramutation, genetic drift, DNA mutation types, Specifically: "no systematic cross species studies of variation have been conducted (most focus on model organisms)", because the topic is so intense.
You don't have to change the DNA code of alleles to go from a chimpanzee to a human, most of the changes come from pre-existing genes that are varied to produce different results.
The texts for macroevolution fine-tuning of variability talk about: variability, gene flow, constriction, epigenetics, of traits of adaptive significance, of DNA mutations, their mathematical measurement... it can be summarized by this statement:
" variability has been a dilemma of evolutionary biology. Considering the pattern of increased genetic variation associated with environmental clines and heterogeneous environments, selection in heterogeneous environments has been proposed to facilitate the maintenance of genetic variation. No comprehensive models have been developed, likely due to the genetic and environmental complexity of this issue. " ref
Many books are devoted to the subject, so there is lots to read through, and there are mutation-control systems that fine tune variability, so it gets complex:
"... Epigenetic modifications, such as; DNA methylation, together with covalent modification of histones, are thought to alter chromatin density and accessibility of the DNA to cellular machinery, thereby modulating the transcriptional potential of the underlying DNA sequence" ref
There are genetic switches, which vary which DNA sequences are expressed by different species... Humans and chimps are 98% the same, and genetic switches can change the species selectively without having to change the DNA itself... "regulates when and where genes are turned on and off and how much protein they produce. The regulatory machinery works when proteins called transcription factors bind to specific short sequences of DNA that flank the gene, called transcription factor binding sites, and by doing so, switch genes on and off." ref
sharks ahve less less variability than humans and 1.5 times bigger genome...
"The researchers found that the white shark genome contained a lot of genes responsible for maintaining genetic stability — things like DNA-repair genes and tumor-suppressing genes. And when the researchers compared the white shark's stability genes with analogous genes in other vertebrates, they found small changes in the gene sequence that suggest a specific pattern of evolutionary adaptation for these genes in white sharks."
Only a few epigenetic processes for transgenerational epigenetic inheritance have been discovered, which vary species traits independently of the DNA sequence, so we don't even know how they compare between animal families.

Interesting Answer indeed. I would suggest reading Cell's argument about yeast as well (on his answer)

In short, no evolution is not a result of variation. Evolution is a process in which each population in a system compete for a limited number of resources and each population has a fitness score (how well suited for the environment they are, this score is a man made concept to help illustrate the point), the populations with a higher fitness score tend to outcompete other species and so they are more likely to survive. This process occurs on a more individualistic level too, individuals in a population can be given a fitness score and individuals with a higher fitness score are more likely to survive and reproduce. Fitness scores are altered by mutations in individuals which may enhance/reduce the function of a certain behaviour/reaction that is required for survival. More advantageous mutations are inherited more often and so accrue within a population and thus over time the fitness score of a population increases too. Mutations are fairly random (they have a higher frequency at certain locations, but it is generally random) and they often occur due to the inherent instability of the bases present in nucleotides. These mutations thus result in the gradual changing of genomes throughout a population, leading to subsequent changes in phenotype - evolution.
With regards to whether an organism ever had 100% accurate copying mechanism, the answer is no again. It is not possible for an organism to achieve this level of fidelity to the nature of the bases used in organism. The DNA bases are inherently unstable due to tautomerisms, deaminations... they can also be altered by natural external factors such as UV radiation which base dimerisation as the electrons in the rings are excited and form new bonds. Although cells have repair mechanisms, these are not 100% efficient as tuatomersiation can occur when the base is in the active site of the polymerase, alternatively, the mutation may occur in a very crowded region in the nucleus, limiting the ability of repair machinery to encounter the DNA by diffusion. Finally, cells are often unable to recognise foreign DNA that has been integrated into their genomes, which will also cause mutations.
Although polymerases have and will continue to undergo extensive rounds of directed evolution it will be almost impossible to produce a polymerase with 100% fidelity unless the bases themselves are changed to being pretty much inert with a ridiculously high stability (remember there are millions/billions of bases in a cell so even if the mutation rate is low there will likely still be some mutations).
In response to Mrigank in the comments (my answer was too long for a comment :/) yeah pretty much  Now it may be possible that we can develop polymerases through directed evolution to have even higher fidelity (although this may be difficult as it could slow down the catalytic rate and then implementstion is alsonhard) and to improve the DNA repair pathways through directed evolution but the bases are inately unstable and there is always some chance of them converting through processes such as tautomerism. Additionally, b cells use a process called somatic hypermutation to actively mutate the DNA of b cell receptors/antibodies for affinity maturation in the dark zone so if we had a system that did not allow for variation there we may have a weakened immune system. Additionally, some repair pathways such as non homoogous end joining don't faithfully repair the DNA they just quickly repair double stranded breaks which can be lethal and this process can result in insertions and deletions. Then at the level of meiosis, since nobody has exactly the same genome and the child gets a chromosome from each parent variation is generated there. Things like viral integration, damage from external mutagens and free radical attack also occur which all lead to mutations. So I don't think it's possible for DNA polymerase to replicate DNA with 100% fidelity and I don't think it's possible in a looser sense for the DNA sequence to not change, hence variation is inevitable.

Thanks fo the direct Answer. So that means DNA can naturally never be replicated 100% accurately and hence variation is inevitable.

Please see the edited answer

Is variation a result of Evolution?

No, you're putting the cart before the horse & mistaking cause for effect.
Variation is the result of mutation (whether caused by copying errors, radiation or whatever).
Evolution is the result of variation.
Mutation > Variation > Evolution
Evolution is merely the winnowing process by which more beneficial variations (as in terms of fittest to survive in the existing environment, which includes competition from other variations) 'succeed' & less beneficial ones don't, it doesn't cause the variations.
Variation can happen without evolution but evolution can't happen without variation.


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What is this grasshopper doing?
I spotted a grasshopper standing on a pavement with a long sting placed in asphalt. I also recorded a video of it moving:
https://youtu.be/JoDdg2yUuYo
What is it doing?

It's its ovipositor & it's trying to dig a hole to lay its eggs.

"How Do Grasshoppers Dig Holes to Lay Their Eggs? After breeding, female grasshoppers dig a hole in the ground in which to lay their eggs by using a special tube in their abdomen known as an ovipositor. The ovipositor is first used to dig the hole, and then to deposit the eggs one by one into the hole"

Probably not having much success on tarmac, did it eventually move onto soil?

Interesting! I didn't see anything left in the pavement holes. Are its eggs visible to human eye? Yes, after a while I pushed it a bit since I didn't want it to stay on the road and it jumped onto the soil but I didn't observe it anymore.

@camillejr : Unless it found a deep enough crack in the tarmac it probably didn't lay anything there, not if it couldn't drive it's ovipositor deep enough, most likely laid its eggs in soil after you moved it.

@camillejr : They should be visible yes.