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If stomatopod crustaceans do not have myelination, why is their reaction so fast?
As far as I understand, there are only two known ways of achieving fast nerve signal transmittance (and hence fast reaction time) in animals larger than ~10 cm: either myelination (as in vertebrates) or really thick neurons (like in cephalopods). However, stomatopods are both quite large and have devilishly fast reaction fitting their predatory lifestyle. They are definitely swifter and more "alive" than lobsters or crabs of the same size (who are all sleepy and slow). However, I have never seen it mentioned that stomatopods have myelination. In fact, this page claims that mantis shrimp (stomatopoda) are not among the few crustaceans that have evolved myelination. Is there any research on how they manage to be so fast? Do they maybe have thick neurons like cephalopods? Or do they have another solution to nerve transmission?

Are you sure these animals have a fast reaction time? Or do they just move quickly or have a specialized high-velocity movement? These are not the same thing. Reaction time measures the time from some stimulus to the start of movement. It does not relate to the speed of the movement.


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How long does it take for a creature to adapt for a different diet?
For the sake of the question, let's say that a population of piscivorous birds are put in a Europe-sized box. Half of the box is sea, populated with their diet of fish and crabs and cephalopods, and the other half is open steppe filled with grasses, bushes and small insects.
Assuming there is nothing else to compete for the open terrestrial niches, how long would it take for these birds to diversify into insectivores, seed-eaters and herbivores respectively? I imagine it'd take very little time for them to become insectivorous, but I don't have a general frame of reference for how long it'd take for herbivory to develop.

Although it may not appear so immediately, I think this is likely a duplicate of: https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont

Have a look at the first sentence in the Modern Research section on Darwin's Finches and read the linked article from there...

source: Stack Exchange

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

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How much dose of mosquito saliva does it need to poison a normal human adult to death, if ever possible?
Image that a normal human adult gets bited by thousands of individual mosquitoes continuously. Will that human adult be killed by the poison(if any) contained in the mosquito saliva injected to the blood stream?

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


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Is APOE present in Lipid Rafts?
What evidence is there that APOE is present in lipid rafts (neurons or glial cells)?
I would be interested in any comparison between the APOE gene variants as well, but that is not required. I've looked around quite a bit for this but could only find apparently the background for a conference presentation (https://alz-journals.onlinelibrary.wiley.com/doi/abs/10.1002/alz.054511). The link is very vague on details.
However, I'm sure someone somewhere has looked at this question...


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How to reduce the viscosity of an extract from a plant seed
I extracted a sample from a plant seed using PBS buffer. The extracted sample is very viscous, even after centrifugation at 15000 rpm for 30 min. The sample is like a thick mucus so that it becomes difficult to do a hemagglutination  assay, and it keeps falling off the pipette tip because of its slimy nature. I can't even estimate the protein content accurately. What can I do to reduce its viscosity?


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Does heterogeneous resistance have an impact on the zone diameter observed in disk diffusion susceptibility testing?
Question
Does the presence of small, discrete colonies within the zone of inhibition, suggesting heterogeneous resistance, impact the zone diameter in disk diffusion susceptibility testing?
"Help us so we can help you"
ASM recommends that such occurrences should be ultimately interpreted as resistance to the antimicrobial:

Distinct, discrete colonies within an obvious zone of inhibition
should not be considered swarming. These colonies are either mutant
organisms that are more resistant to the drug being tested, or the
culture was not pure and they are a different organism. If it is
determined by repeat testing that the phenomenon repeats itself, the
organism must be considered resistant to that drug.
https://asm.org/getattachment/2594ce26-bd44-47f6-8287-0657aa9185ad/Kirby-Bauer-Disk-Diffusion-Susceptibility-Test-Protocol-pdf.pdf

I can't see how this is a sound judgment as there is no way to tell that the persisting variants weren't initially among the inoculum population and didn't appear due to the antimicrobial exposure stress.
Then there is another question: does the presence of this occurrence in vitro also mean that it would ultimately appear in the different in vivo conditions?
Whatever the case, I want to know whether the emergence of such persisters would affect the zone of diameter or not.
It seems to me that it would depend on the mechanism of resistance to the antimicrobial in question: antimicrobials that are resisted by the organism in question through inactivating enzymes are the ones that can be affected. This is obviously because less antimicrobial concentration would be available for the whole population. Then, this is disk diffusion after all not the broth dilution method; organisms have access to the diffusing antibiotic gradient that passes through the part of the plate where they are located.
But if bacteria can't diffuse around (assuming non-swarming bacteria), what about their inactivating enzymes, could they diffuse away from the cells that released them in a significant manner? Then there is another question: shouldn't the appearance of persister colonies alert us to the possibility of additional, unseen microcolonies and could their produced inactivating enzymes affect the outcome of the zone diameter?
Edit:

Still other significant resistances may be subtly evident and appear
as individual colonies in an obvious zone of inhibition (Figure 12-9).
When such colonies are seen, purity of the test isolate must be
confirmed. If purity is confirmed, the individual colonies are
variants or resistant mutants of the same species, and the test
isolate should be considered resistant. Bailey & Scott's Diagnostic Microbiology

Does a purity plate with monogenetic phenotypic variants considered pure in this context?


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Yellow dandelion-like flowers emerging from beach in early spring
What are these yellow-flowered plants?

The yellow flowers look similar to dandelions, but the stalks are much thicker.
No leaves yet, just flowers.
March 30, 2024. Unusually warm winter this year.
Lake Ontario beach. 50ft from the lake. 5ft from grassy embankment. Port Hope, Ontario.
Flowering at the same time as snowdrops and Cornus mas in my garden in a nearby town.

Not certain, but it looks pretty well like it could be Tussilago farfara (colt's foot or coltsfoot). It's a common invasive plant in your area.
https://en.wikipedia.org/wiki/Tussilago
https://www.fs.usda.gov/database/feis/plants/forb/tusfar/all.html

this plant deserves a longer answer with more details,like it is one of the first plants to flower in spring and it is able to increase it`s internal temperature to well above ambient temperature,it makes the flower survive even when there is frost during the nights in spring.

Tussilago/colt's foot is a fascinating plant, and I'm glad you identified it properly. I was unaware of its invasiveness. I was glad to see a patch on my property years ago and sad to see it disappear over the years. (Glad because at the time, I was interested in medieval herbal medicine. Tussilago is one that actually worked. Alas, it's a carcinogen, too.)

@trondhansen - More is nice, but the OP asked for ID. They can learn more by looking at the links, or if you like, you can post a more informative answer.


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How does defining cell assembly by giving weightage to impact caused as opposed to strength of connections change our current paradigm?
Buzsaki, in his paper Neural Syntax: Cell Assemblies, Synapsembles, and Readers, seems to suggest that instead of using synaptic strength and connectivity as a defining feature, a (dynamically changing constellation of) neural cell assemblies could instead be classified based on the impact/output caused by their target "reader" neurons.
Primary question:
Is this an accurate reading of the argument?
His argument, in my understanding, is that the strength of upstream connectivities may not have a biologically meaningful significance unless the downstream potential is interpreted and acted on by the target reader neuron. Hence, interpreting the output/impact caused by the action potential of the reader neuron would provide insight into the nature of transiently formed assemblies as opposed to tracking down the linkages.
Therefore, while the synaptic strength of upstream neural assemblies increases the likelihood of stronger downstream potential, it need not be a requirement as even weakly connected upstream assemblies can gain significance if they activate the target layer. (Hence, the temporal window is a more deterministic classifier).
Secondary question:
Are there any compelling counterarguments to this hypothesis in the literature? Ideally including data supporting one hypothesis or another?

It would be helpful to link to the paper or provide a full reference. I'm not sure the question is answerable with anything but opinion and discussion though. Your post also seems to take as a straw man the idea that strength of connection is otherwise the sole defining feature - is anyone arguing that?

you might consider having this quesiton migrated to the psych/neuroscience SE. That might yield a slightly more relevant/expert group. I also second the suggestion to link the paper directly and try to find a more specific/answerable framing.


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Is there a functional model of the human retina for simulation of conversion of illuminance pattern to nerve signals?
I'm looking for a model that would take a pattern of spectral irradiance over the retina as a function of time and space and convert this into the signals propagating through the fibers of the optic nerve.
I know that there's a variation in distribution of different kinds of receptors over the retina among humans and even between two eyes of a single human, just as there's a variation in the interconnections between the receptors and the outgoing nerve fibers. But I'm interested in a "typical" arrangement that would let me study more general properties of the sensor side of human vision, such as finding different illuminance patterns that yield the same signals after a period of adaptation, or studying how photopic vs scotopic level of illuminance of a scene affects the output signals.
Basically, I'm looking for a black box that would function just as a human retina in terms of input and output.
Is there such a simulator available? If not, has the function of the retina been studied thoroughly enough that I could find a book with enough information to create such a simulator?