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

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

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

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

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

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

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

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


text:
What keeps a muscle fiber in tension?
Someone in massage therapy told me that muscles require some chemical reaction to relax, and that magnesium helps with that.
Looking into it, every source online I've found states that muscles relax on their own.  On one hand, this makes sense because flexing requires energy and our arms would fall to our sides without it.  On the other hand, it doesn't make sense because sometimes muscles hold "tension" (knots) even when they aren't flexed.
I've also read that muscles use ATP only to move, but then have a chemical bond to hold in place (kind of like a ratchet system).  At the same time, running out of ATP will lead to relaxation.  This would indicate ATP is required to keep a muscle contracted.
Conversely, I've read that magnesium helps with blocking calcium, a part of muscle contraction.  This would indicate that calcium is part of some sort of chemical bond.  Chemical bonds tend not to not consume energy to remain bonded.
Other sources state that "muscle tension" is less about the fibers and more about other things (fascia).  That may be the answer to what a "knot" is.
Overall, I'm very confused about what keeps a muscle contracted, and what relaxes it.
If a muscle fiber was contracted in a vacuum, would it stay like that?  Is it chemically bonded in that state?  Or is it somehow held in place by the expenditure of ATP?  Why would the absence of ATP lead to fiber relaxation?

EDIT: thanks to @BryanKrause, the "physiology" section on Rigor Mortis contains details which seem to imply the existence of permanent chemical bonds that require a reaction to release (https://en.wikipedia.org/wiki/Rigor_mortis)

I think there's a good question in here, but I also think it's built on an assumption that a "muscle knot" is a thing that exists and is caused by a muscle that is somehow semi-permanently contracted. Can you cite any reliable source that this is the case? Otherwise, the rest of the question doesn't make much sense, despite all the background reading you've done.

Contrast with: https://en.wikipedia.org/wiki/Hypertonia https://en.wikipedia.org/wiki/Cramp https://en.wikipedia.org/wiki/Tetany https://en.wikipedia.org/wiki/Spasm

Some more relevant information: rigor mortis

@BryanKrause, the only part of this post that is actually a question is in bold; the rest exists to show a bit of the reasoning and information I working from.  Is there anything wrong with the bolded part of the question?

@Darlingtonia.  Amazing!  This does indicate that there is a semi-permanent bond when muscles are contracted that requires "replacing ADP with ATP" or  "breakdown of muscle tissue by enzymes [in death]" to relax.

Possible duplicate: https://biology.stackexchange.com/q/110761/16866

source: Stack Exchange

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

sort: votes


text:
Analysing a microscope image
After a session of practical work in cellular biology, I stumbled across this image of human cheek cells. As seen on the sample below several particles envelop one of the cells. What are they?

The stain: is methylene Blue.
The image was taken by an optical microscope at 40X.
The method of extraction is the following:

These could be:

Small particles of methylene blue crystallizing on the cell's surface
Dirt from the mouth
Dirt from the swab
Bacteria

My best guess is bacteria, since that explains why they are focusing on one particular cell. But one needs more of these occurences to be sure.

bacteria at 40X magnification ?

Yes bacteria at 40x magnification. Clumps of bacteria are even seen in 10x; not at single cell resolution, but well enough to see if cell cultures are contaminated. Hell, you can even see mitochondria in 5x if you stain them.

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


text:
Which plants are best for experiments about plant growth?
I was assigned writing a term paper about optimizing plant growth using control systems. This assignment is part of a class on sustainable energy usage, which means it's primarily on physics and technology.
I will have to conduct experiments comparing the growth of plants under different conditions and whether or not using control systems are effective (and sustainable) at improving plant growth. More focus will be put on the  technical and energy aspects of this problem but getting the experiments with plants right is important, too.
Unfortunately I don't know much about experimenting with plant growth and most of my decisions would be blind guesses. The experiments should be short term (a couple of days would be ideal, the fewer the better. I do still have three months) and on a small scale in general.
The following are some of the questions I have.

What specific plant or species is well suited for what I am describing here?

What are representative and common measures of plant growth?

What kind of light should I use? I will conduct the experiments indoor to keep the conditions about the same each time.

Additionally, I would be glad if someone could point me to good resources on this topic.

With all those questions, you're essentially asking us to design your experiment for you. You should be talking to whomever gave you the assignment for guidance. We don't know exactly what they want. Also, if you want to measure plant growth over two or three days, you would do well to find a plant that grows, oh, inches a day.

why don't you search some experiments for plant growth science, using related words, and see which cress, elodea, tomatoes, grass, and other species they use for different circumstances.

@bandybabboon First of all thanks for your suggestions  <3. I found it quite difficult to find something on this topic because a lot of what I found was targeted at kids, middle-schoolers and suchlike.

as a pre formal researchg you can try gpt frankly, it's pretty detaild if you make it double check and explain.

Arabidopsis is a common model organism for classroom lab experiments, used because of a rapid growth cycle (days is probably too short, but a couple weeks would work).
It would be suitable for proof-of-concept. However, extrapolation to other plants is going to be problematic. There is no substitute in biology for the "real thing", we don't have laws like physics where you can scale using an equation.

I don't know much about experimenting with plant growth and most of my decisions would be blind guesses

The way to answer all your other questions is to read published papers in this area. You'll want to focus on the methods section - something you may have previously trained yourself to ignore, but it's often the most important part of the paper because it is necessary both to understand and contextualize the results and because it is necessary if you want to build on the work done.
If you want a useful project that goes beyond a classroom-level term paper, you should collaborate with someone who does know much about experimenting with plant growth. If you go on alone, you'll probably learn useful lessons about experimental design, but I'd give it maybe a generous 25% chance that you actually answer something useful to your intended research question. Instead, most likely after 3 months you'll have some failed experiments that taught you about ways that experiments can fail which you can hopefully avoid the next time around.


text:
What species does this tooth belong to and how old could it be?
As far as I can tell, this is a single rooted tooth. I suspect (or hope because it would be very cool) it being pretty old, since it is so dark in colour. It is not very pointy, so it doesn´t look like a carnivore tooth to me.
On the picture I think the sequence of the the positional relationship from front left to bottom right is labial, palatinal, mesial, distal.
I'm leaning towards a mandibular incisor. I'm not sure if this could be a human tooth, but it fits size-wise.
It was found on a glacial freshwater lake in Germany. The right side of the scale is in cm.
I would be grateful if anyone has an idea about the owner of this tooth, or could point me in a good direction on how to further narrow it down.

there's a reddit called what's this bone.

Tooth is a good guess, but it's not a human tooth, that much is certain. The root is curved, which would imply (if it's a mandibular tooth) that the mandible is shorter and more curved than ours. My goats had teeth that looked similar to this, but that's not much help, sorry.


text:
Why am I getting a large horizontal band spreading across my native gel?
On every gel of this type that I've ran so far, I'm getting this large band interfering with my gel analysis no matter how much troubleshooting I've done. This is a Novex Wedgewell 6% Tris-Glycine Gel and in each well I've loaded 10ul of the Novex 2X Native Tris-Glycine Sample Buffer + 10ul of my sample. I ran the gel at 100V for 1hr at 4C. This image is from under a Fluorescein Blot filter.
I've troubleshooted the gel by pre-running it and also trying to load without any 2x loading buffer, but the band has still remained.


text:
How to calculate average Corneal Thickness?
I have a question which I may be making out to be a lot more complex than it actually is.
In my department we have a machine which can image the cornea and give values of various parameters (eg curvature, thickness, elevation etc). In particular I am interested in the thickness.
This machine is able to export these values into a .csv file. The data is of all the points of thickness that the machine has measured.
As the cornea is spherical, the data is arranged such that the rows represent radii starting at 0 (the centre) all the way to 6 mm (the periphery) in increments of 0.2 mm. The columns represent meridians of which there are 256, starting from 12 o'clock.
Now the machine spits out data for say the central corneal thickness, but it does not automatically spit out data for the superior, nasal, temporal or inferior peripheral thickness. As such I need to calculate that from the data I have.
I tried to test simply taking all the values for the central 3 mm (ie up to row 1.2 mm) and then dividing them by n (the number of data points) but as expected this did not give me a similar value to the machine calculate central corneal thickness.
I don't have a background in maths or geometry other than A-levels. I am a doctor by training. On doing some quick google searching it appears I need some spaced interpolation method to calculate this but I'm not sure where to begin.
Is anyone able to help me with this or at least point me in the right direction? Is the solution very complex?
Thanks
EDIT
I have attached a diagram with an anterior view, a cross sectional view and an example of how the data is stored in the .csv file
NOTE: the column in the table is meant to represent meridians in degrees, from 0 until 360

I'd recommend starting by sketching out the problem. That is, draw a cross-section of the cornea with how the measurements are arranged and what they physically measure versus what you want to calculate.

Hi thanks. I have drawn out a cross section of the cornea as you say and the method I used initially as described in my question but I am not getting the same answer as what is used by the machine. I suspect this is because I am not taking into account the curvature? I’m not quite sure what other variables I need to take into account to correctly calculate this

Without seeing the drawing or the data or your calculation it's pretty much impossible to figure out where the discrepancy might be.

Hi, I have added a diagram above. I hope this clarifies my question.
Essentially I took data from radii 0 until 1.5mm for all meridians from 0 degrees to 360 degrees to give me the central 3 mm circle of the cornea.
I then summed all of these values together and divided by the number of data points to give me a value for the average thickness.
The value I end up with is between 5 - 20 microns off from what the machine gives me. As such I concluded my method is unreliable.

I don't know what the machine is doing exactly (you could ask the manufacturer perhaps), but you could try weighting the measurements by the circumference at each radius, or the sector area of each radius plus half a step minus the radius minus half a step. The points further from the center effectively cover more area if the spacing is by degree. You could also interpolate a uniform sampling of arbitrary uniform density.

E.g., for points in the 0.4 radius (3rd row), you could consider those to be measurements that correspond to the area between r = 0.3 and r = 0.5. Each measurement in that row then corresponds to area (pi0.5^2/256 - pi0.3^2/256). Measurements in the 4th row would be weighted by (pi0.7^2/256 - pi0.5^2/256), and so on.

Thank you for your help. This was useful.


text:
Why is mean systemic filling pressure used to calculate pressure differential for venous return?
I'm really struggling to understand venous return curves and their relationship to mean systemic filling pressure.
I understand mean systemic pressure is the pressure that would be measured throughout the cardiovascular system if the heart stopped beating and hence pressure would be the same throughout the body and no blood flow because there is no pressure difference.
I'm very confused about the effect of gravity on this, surely if you are standing up the pressure of the blood pooled in your extremities is greater, so is this value just a mean of all the pressures? And I don't understand the usefulness of this parameter, this occurs when the heart has stopped functioning so why do we relate MSP to be a part of the pressure differential driving venous return in the equation:
Vr = (MSFP - PRA)/venous resistance
Maybe my confusion would be resolved if this graph was explained better:

One might notice that during this entire process, somewhere in the circulatory system there is a points which remains at a stable pressure (which happens to be the MCFP),  irrespective of the catastrophic events reverberating through the rest of the organism. Rothe (1993) thought that this probably happens in small venules (less than 1mm diameter), and that it is not constant - present at different points of different organs, and changing constantly depending on prevailing conditions.

I think this means that MSFP might be the high starting pressure in the venules that drives flow towards the right atria and so the MSFP being equilibrated pressure if a heart fails is just that. But I find that arbitrary and entirely confusing.

I think the words tripping you up are "mean" and "systemic". Specifically, it sounds like your intuition is that you should be thinking about an average (mean) across space, across all the systemic circulation, and hydrostatic pressures are dominating your thinking. Probably this is the fault of the person who strung these particular words together, but more generally I'd urge when learning terminology in biology and medicine to not let yourself get fooled by etymology and the meanings of specific words, but rather to treat terminology as terminology.
Instead, I'd think about this as it's usually measured, which is as a pressure at the venous return with the heart stopped. For "mean", I would not think of this as an actual average in the typical sense, but rather just as a steady-state, when there is no pressure differential between veins and arteries, rather than no pressure differential between head and foot.
Physically, MSFP represents the pressure of the compliance of the vasculature. Blood vessels are not hard plastic or metal pipes, they are flexible and muscular, and they push on the blood inside to create a pressure even without any pumping or anything. That's what MSFP is trying to measure. Don't forget that in physiology we are nearly always talking about relative pressures rather than absolute; we don't think of the approximately 760 mmHg of atmospheric pressure when we measure blood pressures in the range of 10 to 200 mmHg, there's always a reference point, usually the immediate vicinity outside the vessels/outside the body. That would also be a good approximate reference to the pressure in an "empty" heart, so if you measure the pressure right outside the heart at a steady state, it gives you an idea of on average how much tendency there will be for blood to flow into the heart if it were empty.
I hope that's helpful, you might try to read more from other sources if your textbook isn't quite clicking:
https://en.wikipedia.org/wiki/Mean_systemic_pressure
https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04024-x
As far as hydrostatic pressures, I think you're not seeing them discussed in this context because they just aren't that relevant to this particular static model of what is happening to blood at the level of the heart due to passive tension and blood volume in the vasculature. I'd set it aside and learn separately about how blood flow overcomes hydrostatic pressures particularly in the legs through valves and pressure generated by surrounding tissues.


text:
Do technological developments terminate the evolution of human species?
One of the most agreed upon mechanisms for evolution is natural selection. Changing environmental conditions necessitates development of variations that enable the survival of that particular species. These genetically passed down variations later becomes the adaptive features which further result in the development of new species.
But with the development of technology we are finding newer ways to cope up with changes in the environment. Does this impact human evolution?

please search for similar questions before you post, this has been asked several times. https://biology.stackexchange.com/questions/20291/human-evolution-in-modern-times

"Natural selection" is a somewhat misleading term.  Evolution does not need "natural" selection to occur; it only needs selection.  Even the term "selection" is a bit misleading because it's often thought of as referring to the death of individuals or, somewhat more accurately, as reduced likelihood of producing offspring, due to lower fitness.
In fact, any process that gives individuals with particular genetically determined features - a reproductive advantage in a given ecological niche will drive evolution among the sub-population within that niche.
Addressing your question more directly: Suppose technology leads to people whose keyboarding talents are high having more children.  If so, it will tend to drive evolution among the sub-population having access to keyboards toward genotypes having higher keyboarding talents.  But if having keyboarding talents results in those individuals having less likelihood of producing children, evolution in that sub-population will be driven in the opposite direction.
IF it could be said that technology in general decouples human reproduction from "natural" influences like disease, resource availability, climate, etc., it could then be said that evolution will be less driven by those influences and more driven by, e.g., the cultural tendencies of particular sub-populations to produce more children.  But that would be a gross over-simplification.
It is almost certain that changes in technology have had significant influence on human evolution.  Agriculture, clothing, tool use, etc., have all had long-term consequences in human evolution.
Human culture is very complex, and separating out all the effects of technology on differential reproduction rates among sub-populations would be extremely difficult; but it's almost certain that there are such effects.

You might enjoy the 2006 comedy, "Idiocracy". The premise of this movie is that while technology allowed every person to survive, the smarter people study more, have a more demanding career, and have fewer children than the stupider people who just have a lot of kids - and the hypothetical result is that in 500 years, the human population becomes much less intelligent than it is today. Of course, this is just a movie :-)

It was a fun movie, and I refer to it often.  Just a movie, yes.

Evolution is not a path towards perfection/improvement but simply a series of changes over time.
Thus, as McGrew explained, technology can have an effect on what drives our evolution but cannot stop evolution: nothing can actually, because changes happen even by simple chance (see e.g. genetic drift).

Arguably it is possible that technology will stop human evolution.  Technology led to burning large amounts of fossil fuels, which causes global warming.  If carried to an extreme, this renders the Earth uninhabitable for humans (and most vertebrate life forms).  Thus technology renders humans extinct, and since extinct life forms don't evolve...


text:
Looking for specific alga and a recently extinct (or rare) marine animal from the same region for novel
I'm writing a novel where there is a drowned body in an inland lake. The idea is that she was drowned after a fight in a container containing sea water for smuggling a recently extinct (in the novel, supposedly extinct) or a rare marine animal, and there was also some species of alga in her lungs.
Hence, I'm looking for two species from the same ocean or sea (endemic or not), where some info on the genome is known. The best thing (or you tell me if it makes sense at all) I could come up with so far is the Great Auk (Pinguinus impennis) and brown alga of some species which I think is mostly found in the North Atlantic.
Very grateful for any info on the genome (no details necessary, just whether the DNA has been sequenced and whether it would be possibly to identify by a tissue sample), chromosome number and other info on the great auk and some Phaeophyceae alga or any other input for a fitting pair of species. My novel is set in 1994, and they identify the species by forensic PCR methods, no need for a specific match, but by a shred of skin or so I need two marine species identified (not with 100% certainty, good odds or a near-match is enough) by some forensic way, can be anything really, one of them small enough to be in the water in the lungs of a drowned body. Or a genus could be enough, the plot element is just that she drowned in a container used to transport an animal.
Sorry if it's inappropriate to ask this here, it's not a scientific question I know, but I trust I get the highest quality input here.
Actually, the alga is of secondary priority, if someone could point out a recently extinct marine animal which can be matched by its DNA, or by a tissue sample using some other method, I can even scratch the alga, but it would be a nice cherry on top.

Yes, at least some of the genome has been sequenced for the Great Auk (Pinguinis impennis): Taxonomy browser @ NIH (click on the 45 next to the Genomic Sequences title). There appear to be 45 different genomes published. All of them are mitochondrial genomes, which are relatively easy to reconstruct, as well as super abundant in any tissue. They can be used to identify samples to the species level.
I don't know of any specific algae that might match, as these tend to be very widespread (as one might expect for a marine species that is distributed by currents). You might be able to concoct one fresh-water one that comes from some remote island where the Auks are found. Perhaps a land-bound plant pollen or spore (moss, fern) in the lungs instead if she has been collecting these animals from somewhere? It doesn't have to be real after all, just believable (for example Dan Brown's Da Vinci Code theories etc.)!

You might find this Telegraph book review fun (best book review I ever read): Don’t make fun of renowned Dan Brown.

@anongoodnurse I think I have seen that before, or perhaps a similar one about another author, still gets a laugh out of me.

Hey, thanks a lot for the input! I guess the Auk will do then with your confirmation that it can be positively identified by the mDNA -- But, @anongoodnurse, just asking out of curiosity (and thanks for the funny review, or whatever it is, I assume I'm missing out on something, his constantly referring to himself as renowned I assume); is it that (a) this part of the plot sounds so far-out it reminds you of Dan Brown or (b) my grammar or style reminds you of Dan Brown or (c), heaven forbid, both?

It will be much more far-out pulp stuff than Dan Brown, but with a tiny difference: the book won't take itself seriously. Or so I hope. So heaven forbid anybody associate my grammar or style with Dan Brown, that was my point, although I'm writing the first version in German, so I'm off the hook for the time being.

@bob1, however, has this been sequenced in 1994? I understand PCR was fairly new then so you'd need a huge sample? Could they run as many cycles as they do today? Also, the genome is only 16k base pairs and 10k are identical, is that correct?
Sounds like nothing, I thought humans have several billions and the onion (I heard) has much more...? But most of it is junk anyway, or so they claim?

@FissionChips PCR is largely unchanged since the 90's, besides some advances in detection technology, mechanization and enzymes, the reaction used today is the same as Kary Mullis invented. I was doing PCR in the late 90's on machines that are still sold today. Sequencing - massive advances since the 90's. Sanger sequencing (chain termination) is still common and largely unchanged since the 90's too. Both definitely possible and quite sensitive even back then. Wouldn't have been able to do sequences off historical things back then though, ancient DNA tech has come a long way.... cont

cont... Those are mitochondrial genomes (~16k bases) and all from the same species, so about right in terms of diversity. These will be distinct from other species though, at least in the right regions, so is very useful for species ID. These were 4 mtDNA genomes generated in 1994 -see fig 2 and section "early mtDNA discoveries" for more info. Earliest were 1980's, so it isn't out of the realms of possibility to have had great auk there, it's jsut that people focussed on easy (abundant) species first.

@FissionChips I mentioned Dan Brown as an e.g. of someone who gets the details wrong, but still tells a story that is believable. Your has to stretch the tech and knowledge a bit to get Great Auk sequenced in the 90's; the ability was almost there, just people hadn't got around to it. Another e.g.: I remember reading a fiction novel in early 2000's about a person with dwarfism who modified an embryo and implanted it in a woman so that the child would carry his form of dwarfism. We weren't capable of doing that sort of thing at the time of setting, but still an interesting read.

@FissionChips - No, not at all! Actually I upvoted your question because that sounded like a fun twist. I only posted that review because Dan Brown was mentioned and it's so on-point about his writing, which is terrible. I doubt he could have written the question you wrote as well as you did. :) He has his fans, though, which is fine by me. I'm not high-falutin (sp?), though. I read The Silmarillion, but actually had to take notes to keep things straight. Could not finish Foundation, though I love Asimov. Too complicated for me.


text:
What is happening to this moth cocoon?
We 'adopt' a catepillar each year and this year I believe we have a Buff Ermine Moth.
It seemed healthy and created a woven cocoon. It was at this point that I found out these moths overwinter.
We put it outside when we started to use the heating again to avoid it drying out.
Within 24hrs of being outside, two hard areas appeared outside the cocoon, actually poking through the dried leaf to which it is attached.
The following day one of these hard objects fell off!
This is completely different to the other catepillars we have observed and I wondered what is going on. Is the catepillar still OK??
Photos attached.
Thanks for your help!
Just to note, the woven cocoon is actually between those two leaves. It's not that clear on the pictures. The cocoon itself seems unaltered.

Maybe it died. Seems kind of like insect abdomen.  But I am not the expert


text:
how many bipolar cells connected to a ganglion cell?
Is it that only one bipolar cell is connected to one ganglion cell (which (ganglion cell) is connected to only one LGN neuron cell)?
I mean if more than one bipolar cell is connected to a ganglion cell, then how can the ganglion cell be ON or OFF center? Because what if two ON center and two OFF center bipolar cells are connected to the ganglion cell? Is the ganglion cell ON center or OFF center? Thanks in advance!


text:
why do we use the glasses so that a different image is seen in each eye in the binocular rivalry experiment?
If we use the glasses so that in the right eye we see a house and on the left eye a face, we can see with a fMRI that the FFA is activated when seeing the face and the PPA activated when seeing the house. But if we did not use these glasses and just saw the house and face superimposed, how would the recording look? The recording for when you force yourself to see the house and then the face? The same as with the glasses? So what difference do the glasses basically make? Thanks in advance!

source of image: https://www.sciencedirect.com/science/article/pii/S0042698909000169

It would be helpful to include references/sources in your post. I would expect the source to explain the purpose of this experiment, what have you read and why does that explanation not make sense to you? I'm not really understanding what you mean by "just saw the house and face superimposed"; how would that happen, exactly, without the glasses?

I included an image into the post! That is what I mean by seeing the house and face without glasses, so you would see them simultaneously and only one of them if you force your brain to perceive only one of them.

How would that show binocular rivalry?

aah wait, so binocular rivalry is created when your brain perceives two alternative images because both eyes SIMULTANEOUSLY see something different.  Without the glasses, you would be able to control what to look at, there is no alternation of images as one image is perceived at a time. If we see the face by the right eye, I assume the right temporal retinal fibres do not participate for perceiving the image because that is for the left visual field, right? And so this means right temporal and left nasal retinal fibres do not get involved in this binocular rivalry experiment with glasses?

I'd recommend backing up a bit and looking at the big picture. What's the whole point of these experiments?
Binocular rivalry is an observation, like seeing that the sky is blue is an observation. That is, when you present two incompatible images to the two eyes, you typically perceive one or the other, not a combination: that's the observation/phenomenon.
The next step is to use this observation to try to understand more about how the brain processes information. Not necessarily just to understand this weird binocular rivalry paradigm, which isn't something that would normally occur out in the world (without someone messing around with some goggles your eyes are generally going to be viewing the same world, not different ones), but to ask how this little "malfunction" gives insight into how the brain processes information in general.
An fMRI experiment that shows the FFA is activated when someone perceives a face, and PPA activated when someone perceives a house, tells you something about the relationship between PPA and FFA and perception. The context of binocular rivalry presents an interesting and very useful control experiment.
Let's set binocular rivalry aside for a moment and just consider looking at pictures of houses and faces. Again, you'll see differences in FFA versus PPA with houses versus faces, great. But, you'll also see differences at the retina. In fact, if you had some machine learning algorithm, you could definitely use responses from the retina directly to figure out if someone is looking at a house or a face: it's really the same problem as doing it from a camera image. So, this test isn't really measuring anything about what's going on "inside your head"/inside the mind/conscious perception, its just measuring a biological representation of the outside world.
Now consider binocular rivalry: you're presenting a constant face image to one eye, a constant house image to the other eye. At the level of the retina (and, to some extent, in early visual processing areas in the brain like LGN and V1), you can expect exactly the same activity no matter what the perception is: the experiment lets you dissociate what is different because the perception is different from what is different when the outside stimulus is different. The outside stimulus stays the same, yet the perception changes, and the perception changes are associated with changes in activity in particular brain regions. That provides some evidence that perception of objects (rather than mere signal processing of visual patterns) involves brain regions like the FFA and PPA.


text:
How does retinal ganglion cell receptive field affect the LGN neuron activity?
If we have a spot of light hitting the center of the ON center receptive field of a retinal ganglion cell, will the LGN neuron be activated? Will the V1 neuron be activated? I mean its receptive field looks different, see the image below. I am just so confused on what the receptive field of an LGN and V1 neuron even means. In other words, how is the receptive field of the retinal ganglion cell related to or how does it affect the receptive field of the LGN neuron?
If light shines in the center of the ON center LGN neuron receptive field that is not in the receptive field of the ganglion cell, then the LGN neuron is activated and the ganglion cell is not. How does that work? How can it skip a stage? Does not the RGC first need to get activated for the LGN neuron to get activated?
Since a V1 neuron to get activated for example needs a shine of light that is 45 degrees diagonal to the right, will it get activated if only a spot of light is shone to the ON of the ON center retinal ganglion cell? This RGC is connected to the V1 neuron is it not?
In conclusion, I think that I am confused in why is the ganglion cell connected to the LGN cell, which is connected to the V1 cell, when they all have different receptive field. What does the connection bring about?
Thanks sm in advance!

The picture is showing you how receptive fields are combined at different levels of the visual processing hierarchy. The activity of multiple cells is combined to influence the activity of the downstream cell. This diagram is a bit confusing in that it focuses only on one RGC to show divergence (connection from one to many from the RGC) from RGC to LGN and then only convergence (connection from many to one in V1).
Light doesn't only shine "on the receptive field of a retinal ganglion cell"; light shines on some spot on the retina, which will influence multiple retinal ganglion cells. If you want to understand what happens at the level of LGN or V1, you need to consider all of the inputs to a cell, not just one of them.

If we have a spot of light hitting the center of the ON center receptive field of a retinal ganglion cell, will the LGN neuron be activated?

Maybe? Who knows. Neurons in the LGN will be activated (fire action potentials) if they receive enough excitatory input (and little enough inhibitory input). If you have an ON-center RGC that synapses on an LGN cell, then yes, light at the center of the RGC receptive field will increase the likelihood that the LGN cell fires.

Will the V1 neuron be activated?

Maybe? Who knows. If light only lands on the center of one of the LGN cell receptive fields, it's also landing in the "surround" of the other adjacent LGN cells that also give input to V1. You'd expect the V1 neuron to be more active in response to a spot of light than if light only fell in the dark surround area, but far less active in response to a spot of light than to a bar/line of light that looks like the shape on the right hand side.
I would recommend working back the other way. Look at the way the receptive field is drawn: that tells you how light in different areas will influence that cell's firing. Light on the white background areas increases firing, light on the shaded areas decreases firing. Then, work backwards in the pathway to understand how those responses could have been created by adding together cells at the previous level of the processing hierarchy.

What does the connection bring about?

No light shines on any cells in the LGN or V1. These are deep in the brain. Light information needs to be transmitted to them in some way. Without connections between these cells, there would be no responses to light in the brain.

Whoa! Thank you so so much! So nice of you to spend so much time answering my questions to help me out, I greatly appreciate it

there is only one ganglion cell connected to only one LGN cell? But more than one LGN cells connected to a V1 cell? Does the receptive field of a ganglion cell superimpose with the receptive field of the LGN cell to which it is connected? Are their receptive fields identical? If not, lets say if that of the LGN is bigger and light is shone on a part that does not shine on the receptive field of the RGC, then how is the LGN cell activated when RGC is not? Since only this RGC is connected to that LGN cell so it is the only one that can activate the LGN cell (?)

and since V1 cells are only activated by bars of light, then if I am seeing a round spot of light, is any of my V1 neurons being activated?

@Maria Each RGC connects to multiple LGN cells; each LGN cells receives input from multiple RGCs. Each LGN cell connects to multiple V1 cells, and each V1 cell receives input from multiple LGN cells. There are also lots of different types of V1 cells and receptive fields, arranged in different layers of cortex; only the "simple cell" is being depicted here.

V1 cells are activated best by bars of light. How V1 will be activated will depend on the size of the spot of light; if it's small then yes, any V1 cells where that spot would fall on their 'bar' would be weakly activated. If it's a big circular spot of light, you'd expect V1 cells to be activated in a pattern consistent with a line of "bars" along the edge of the circle in a tangent orientation, where light lands on their center and one side of the surround, but not the other side. V1 receptive fields are also considered "edge detecting".

I highly recommend reading some of the early papers by Hubel and Wiesel that show how people learned these things before any of it was known by anyone.

cool! thank you so much! sorry to bombard you with qs, but how can an LGN cell be an ON or OFF center if it receives input from many ganglion cells that can be a mix of ON or OFF center? I thought that it went like if the bipolar cell is ON, the ganglion cell will be ON, and hence the LGN cell will be ON

@Maria I'm not sure whether LGN cells do get a mix of ON and OFF input, is there a reason you think that's the case? Hypothetically, there would be nothing wrong with assembling an "on-center" receptive field by summing aligned on-center receptive fields with offset off-center receptive fields, but I don't think this actually happens until V1.


text:
what does concentric antagonistic areas in the retina mean?
"concentric antagonistic areas seen in retinal and LGN receptive fields." (Source: Neuroscience: Exploring the brain)
So the receptive field of a ganglion cell is either ON or OFF center. What does this "antagonistic area" mean in the ganglion cell receptive field?
I did not know that the surround can be called ON or OFF, I thought it was just the center. Doesn't the OFF and ON for the center stem out from depending whether the bipolar cell in the center is connected to the ganglion cell is either an ON or OFF bipolar cell? The photoreceptors in the surround are connected to the same bipolar cell (image below).

Image sources: https://azretina.sites.arizona.edu/node/241
https://nba.uth.tmc.edu/neuroscience/m/s2/chapter14.html

Antagonistic means opposite/opposing.
The receptive fields have ON and OFF areas that oppose each other; that is, light on the surrounding area has opposite effect of light on the center.
It gets clumsy to always say "on-center off-surround" or "off-center on-surround" to describe bipolar cells or retinal ganglion cells, so when you hear "on" or "on-center" to describe one of these cells, this is just shorthand for "on-center off-surround".


text:
Does thermal shock apply to human bones?
I always knew that a drop of cold water would crack a hot glass. But does this apply for our bones tho? Obviously not instantly, but after repeating it for years?
I've always wanted to do cold showers and drink cold water but I instantly have these annoying thoughts that my bones would crack overtime or that my teeth would shatter.
A phobia of a thermal shock I guess.
However, I see people do ice plunges and spill iced water over themselves, and Islam makhashev going from laying on ice to the sauna: https://youtube.com/shorts/XFW29nSowAw?si=BkySqtRf2bKm5pjA
So I just wanna know does thermal shock apply to our bones? Would going from hot to cold or vice versa damage the performance of bones and joints eventually?
Also, I especially mean the spine. I Litterly cannot stand the thought that doing a cold shower would make my back like an old man's. Squicky and painful to move.

No is the answer to this - stop a think for a little bit. If this were the case, there would be many thousands of such incidents observed every year, and no-one would ever do such things as plunge into ice-cold water (there are plenty of videos of this on YouTube) or visit cold climates. Bones do not behave like glass. In addition, your bones are inside your body, where they are heated by your blood and body mass. Thermal shock does not apply.
Teeth on the other hand, can crack from cold, but it needs to be very very cold, much colder than you will ever experience unless you are visiting Antarctica in the depths of winter, or perhaps parts of the Arctic (Yukon, Siberia) in winter.
As far as I know, the only documented cases of this happening, happened to the members of Scott's Terra Nova party who went to Cape Crozier in the middle of winter to collect Emperor Penguin eggs in 1912. This was a side scientific quest apart from the attempt to be the first people to visit the South Pole, which was the main aim of the expedition. The best description of this trip to Cape Crozier is described beautifully in Apsley Cherry-Garrard's 1922 work The Worst Journey in the World (it is well worth the read, one of the best written memoirs ever).
During this voyage, the temperatures fell so low, that they weren't able to measure them accurately, but definitely below -75 F (-61 C), and resulted in their teeth cracking. For some frame of reference, your domestic freezer, where you might keep ice-cream and frozen meat runs at about -4 F (-20 C).  I suspect this was a result of a number of things, not simply cold - first and foremost being dental hygiene, which was rudimentary at best in those days. Secondarily, they had poor diet while sledding in particular, so might not have had the strongest teeth. They also were very cold (so cold they had ice inside their sleeping bags) continuously for about 3 weeks, so were chattering and/or clenching teeth almost always, so putting a lot of strain on their teeth.
To quote the book from a couple of places:

They talk of chattering teeth: but when your body chatters you may call yourself cold. | can only compare the strain to that which | have been unfortunate enough to see in a case of lockjaw...

...I don’t know why our tongues never got frozen, but all my teeth, the nerves of which had been killed, split to pieces.

Now this is exceptionally rare. You are very very very unlikely to experience anything like this, under conditions of hardship such as these men experienced, certainly not from drinking cold drinks or taking a cold shower.


text:
How are plant meristems free from viral infection?
My textbook mentions an application of tissue culture; A meristem extract from an infected plant (both apical and axillary work) can be used to grow a virus-free plant in vitro. But what makes these meristematic cells special so they don't get infected?
Edit:I read an article on a protein called WUSCHEL that inhibits the prodction of viral proteins (by halting protein production altogether). So is this protein the main reason?

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. Please also note the homework requirement - so tell us what you know about this topic - hint: there are lots of answers easily accessible by searching.


text:
If both parent squash are edible can the child squash be toxic?
Assuming contamination from a toxic squash didn't occur, could cross pollination of two edible squashes be toxic?

Please [edit] your question and explain what you mean more clearly. How would the hybrid be produced? Breeding? Genetic manipulation? What kind? Are you thinking of specific, known toxicity that already exists in other cultivars/species? Are you talking about general toxicity, including novel traits?

Hi Dave, thanks for editing your post; I think terdon's comment is very important and I encourage you to read and consider it in its entirely: so far you have only responded to one part of that comment. It might be especially helpful to link to what you've already read about squash toxicity that has led you to ask this question.

easily, see stress induced gene expression in Cucurbitacin


text:
Mapping Ion Channel mRNA Copy Number to Channel Conductance
At least in invertebrates, it appears that within identified cell types, there are robust correlations between ion channel mRNA copy number (as identified by single-cell qRT-PCR) and the maximal whole-cell conductance for that ion channel species. For an example, see the following paper:

Variable channel expression in identified single and electrically coupled neurons in different animals (Schulz et al., 2006)

These results suggest that in general, we can model the relationship between ion channel mRNA copy number $m$ and conductance $g$ as
$$ g = \alpha + \beta m + \epsilon $$
where $\epsilon$ is some noise term and $\alpha$ and $\beta$ depend on cell type and ion channel species. In general, one would need to fit these parameters from data. I have two questions:

Due to issues with capture efficiency, etc., is it reasonable to expect there to be similar linear relationships between UMI counts of ion channel transcripts from scRNA-seq and ion channel conductances? Or is only qRT-PCR sufficiently accurate for estimating copy number?

If one does not have conductance data available to fit a regression model, are there theoretical models (e.g. involving gene regulatory networks) from which one could derive expected mappings between ion channel copy number and conductance?

I don't have access to the paper so I can't fully evaluate the relationship you describe. I'm also neither an electrophysiologist nor a
However to answer your questions:

This to me is a solid "probably?". It is reasonable to expect a correlation, but that doesn't mean that one will exist for any given mRNA species, especially given the rather noisy nature of scRNA-seq data. (Maybe it's gotten better more recently, I haven't tracked the tech closely). Briefly, RT-PCR will almost certainly be more accurate, but scRNA-seq will probably approximate the same answer (one possibly helpful though slightly old reference).
I'd be pretty skeptical of such a model constructed without regard to empirical conductance measurements. I can readily find people claiming to have accomplished something like this. These models are directly based on conductance measurements so they are likely somewhat trustworthy, and their fit to data appears to be pretty good (see figure; I have only the vaguest idea of what's being plotted here, so read the paper!)

Thanks so much, this is really helpful. If possible, could you update the second link you posted? As of now, both links are identical, leading to the same "Briefings in Functional Genomics" paper. If not, no worries. Thanks again.

@nguzman sorry fixed


text:
Bacteria genetic screen for mutants
Is there a simple screen for bacterial mutants with increased mutation rates? For example, detection of some loss-of-function mutation that causes increased mutation rates.
Any screen I can think of (for example, just testing on several different selective mediums) would select for bacteria with several mutations, but that does not necessarily imply an increased mutation rate.

You may give a look at the Ames test, and possibly adapt it to your needs. Basically, the test was developed to identify genotoxic substances, i.e. substances that increased mutation rates in bacteria.
The standard way is to use strains of bacteria that are classified as His-, i.e. they need an external source of Histidine to survive.
In the Ames test you prepare two cultures of such bacteria. One of them is exposed to the hypothetical mutagen, and one acts as a control. You grow both of them in plates with minimal amount of Histidine, so that all bacteria grow for a while.
When Histidine is over, only the revertant mutants will survive. If the hypothetical substance is a mutagen, you should notice that in the corresponding plate there are more revertant.
This can be easily adapted to your case if your strain are His- (or can be convinced to become His-) or have some other identifiable mutation.
So, assuming that you are happy to compare mutation rates in a series of strains that are His-, you just need to compare the growth of those strains on minimal histidine and the faster growers are likely those with the higher mutation rate, according to Ames postulate.
If your strain do not have such a property, it may be more difficult (and actually, I wouldn't know what to do, right now!)


text:
Why are trees so symmetric?
Many trees have a quite symmetrical overall shape. Some are extremely symmetric. Yet when you look at the branches and limbs of any tree their distribution seems completely random. Often even the trunk will bend or divide. So how does the overall shape attain symmetry?
I understand that there is gravitotropism and phototropism acting, but it seems to me that then if one branch extended outside of the general canopy it should grow even faster as it is more exposed to sunlight, thus producing a more irregular shape.
What mechanisms are working here?
There must be some kind of negative feedback (I'm a retired engineer) or inhibitory mechanism that slows growth on the more exposed branches.
I can understand that a spruce or similar would be so. If all the branches grow at the same rate, those lower on the tree will be longer, having had more time to grow and you'll naturally get a triangular shape, but this is not what captured my attention.

"...if one branch extended outside of the general canopy it should grow even faster as it is more exposed to sunlight, thus producing a more irregular shape." Are you sure this doesn't happen? (It won't happen with one branch, but it will generally on that side of the tree.)

if you think trees are mostly symmetric you need to go look at more trees, and then look up phototropism. a unobstructed tree with light levels the same in all directions will be symmetric sometimes, otherwise no so much.

@anongoodnurse That's true. I have two maples in my front yard growing close together. There are no branches that grow on the sides of the trees facing each other - and yet the two trees together make one symmetric whole.

In PA the sun spends a lot of time in the morning and evening in the north half of the sky during summer thanks to the Earth's tilt.

@BryanKrause You're right. Never realized that.

Perhaps set a condition of trees growing without light obstruction and high wind. Conifers are very simmetric and so are other trees. You should read about the chemical signalling which tells each cell it's distance from the trunk and how targeted growth is promoted.

@Rich - I built a house in the middle of acres of woods, clearing the site myself. Ten years later, the trees left standing on the entire periphery of the clearing grew into the clearing so much that I had to cut them down to regain the sunlight I originally had. I don't think I'd have known it was so dramatic if I hadn't seen it myself.

@bandybabboon That is the sort of information I was looking for. Can you give me a reference for this type of chemical signaling?

Does this answer your question? How do trees manage to grow equally in all directions?

@NilayGhosh Yes, that's a very complete answer. Thanks. Knew there had to be some kind of regulatory feedback going on.

Not an answer, but the history of people investigating spiral patterns of plant growth may be interesting to you.


text:
Stealth Mosquitoes?
Have mosquitoes become silent and invisible, or am I losing my senses of hearing and sight?
This summer I have seen no mosquitoes and have only heard two of them, very quiet, as I sat on my sofa late at night and as they buzzed around my ears. And yet I am consistently bitten, often on the back of my hands and on the front of my forearms (where I should be able to see them feeding) whenever I go out. I don't see them, ever.
Previously I have caught mosquitoes as they fed on me, but this year not.
I live in Allentown PA. Is there a new breed of smaller, quieter stealthy mosquitoes, or what?
EDIT with new image
Following @anongoodnurse advice I have seen a killed four of these in my kitchen. Formerly I had disregarded them as harmless little bugs, because they were silent. I saw that they were definitely mosquitoes, but very small and very black. Two of them became black splots on the wall, the fourth looks like this:

It definitely has white stripes. This one is about 4mm long. They fly very slowly, and are completely silent. I swatted this one on my hand.

I'm up north of you in NY.  It has been a quiet mosquito season until the past few weeks.

@rtaft Noticed the same here. Don't know if mosquito activity was reduced during the hot weather, most likely it was because I didn't go out.

Definitely genus Aedes, maybe A. japonicus (less white than the Asian Tiger, A. albopictus)? Nice update!

Your sight and hearing are probably fine. You might be experiencing the relatively recent population growth of Asian Tiger Mosquitoes, a tiny, quiet mosquito that first appeared in Houston, Texas in 1985.
From the PennState Extension:

Over 60 species of mosquitoes can be found in Pennsylvania... Two invasive mosquito species, the yellow fever mosquito (Aedes aegypti) and the Asian tiger mosquito (Aedes albopictus) have been found in southern Pennsylvania; however, their range may change and move further north.

From the French Agency for Food, Environmental and Occupational Health & Safety, it is:

Noiseless and diurnal: in contrast with the common mosquito (Culex) which tends to bite at night and which makes noise when flying, the tiger mosquito is diurnal, in other words it bites during the day (mainly in the morning and the evening), and it makes no noise.

Small: This species of mosquito is actually quite small, less than 5 mm in length.

Black and white stripes: ...the tiger mosquito is not yellow and black but white and black.  It is also characterized by the presence of a white dorsal line along its thorax. Its legs also have stripes.

In Southcentral PA, I am only two counties west of you, so not far. Mosquitoes don't seem to be particularly attracted to me, and the few times I've been bitten this summer (on my forearms), it was a complete surprise, and by the time I realized it the mosquito was becoming engorged. More frustrating is that each time it was during afternoon daylight, a time which used to be mosquitoless. They were Asian Tiger Mosquitoes.

I'll keep an extra close eye open for them.

More of a joke than a comment but ability to hear high frequencies decreases significantly with years aged even in young, "healthy" individuals (i.e. Wang et al, 2021) so it might very well both be new kind of mosquitos and a (slight? subclinical except for those damn mosquitos?) decrease in hearing compared to the year before :)

@Narusan Could be. They are much smaller than "regular" mosquitoes and their rapid wing beats might put the sound frequency up near ultrasound range. As I mentioned I have heard mosquitoes in the quiet of the evening, in my living room.

I've lived in Texas most of my life, and to me these are regular mosquitos! I guess that explains why I never really heard the stereotypical "mosquito noise" much

@RadvylfPrograms Oh my word! I've only ever heard the high, annoying whine of mosquitos until a short few years ago. At least it was a warning to beware. These little creatures take me totally by surprise!

Finally tracked the little blighters to their lair. They have been using the water in our lucky bamboo to hatch their nefarious plots.

Translation of mosquito whine:  This won’t hurt a bit. There may be a little discomfort later: swelling and itching. Just remain calm while I take a small blood sample.  (In a small percentage of operations there may be serious side effects: West Nile fever, dengue fever . . . . .)

@anongoodnurse Sincere thanks to you. Previously I had seen these small flying bugs which I considered slightly annoying but innocuous and had just waved them away. Since receiving your answer I have assiduously hunted down and swatted eight of these in my home. As a result, rather than being bitten two or three times every day I have only been bitten once in the last two days, the perpetrator of which is in the photo in my question.

@Rich - My pleasure! I learn things, too, when I answer, like how very little water these things need to reproduce. I was surprised and chagrined; I found that they were breeding in a tiny pool of water that collected in a broken piece of pottery in my garden (which I had been watering due to the heat). I've been supplying the neighbors with mosquitoes without realizing it. So we both got more than just "reputation" points! :)


text:
What is this small black bug found in Turkey?
What species is this? It was found in Turkey. It was dead, I did not kill it.

Looks like a scarab beetle (Coleoptera, Scarabaeidae). Species is difficult to tell without better pictures, but perhaps Scarabaeus typhon?
Edit: OP has IDed in comment as Scarabaeus jalof

@Oğuzİsmayiluysal If you think this answer is correct, we encourage you to accept it.

Definitely looks like a member of Scarabaeus but why S. typhon?

@augurar I forgot to edit my comment it is not typhon. It is a S. jalof. https://c4.staticflickr.com/4/3510/3847992837_b3aa34f400_b.jpg

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Cause-and-effect questions about growth and development of plant
I need to solve some cause-and-effect problems. The problems are related to growth and development of plant. "Growth and Development" chapter is the first chapter in third level of high school (senior high school).
Show your answer with "Is the statement true?", "Is the reason true?" and "Are the statement and reason have cause-and-effect relationship?"
Problem 1

Anthurium should be sprayed with cytokinin hormone to prevent from wither easily.
Reason
Cytokinin hormone promotes/stimulates the growth of axillary buds that will produce lateral branching.

Problem 2

The stem of Avena sativa with the coleoptile is being cut, couldn't elongate.
Reason
Phytohormone that used for growing is only available at the end/peak of coleoptile.

My attempts to those problems are here:
Problem 1
What I know about cytokinin is when you soak the green leaves in the water with cytokinin, the green color will stay longer than without any soaking. I don't have any idea about the effect of cytokinin to flowers. I think I need to dig more knowledge about the hormone.
I'm not sure with the reason too. Quick searching in Google Cytokinin and Wikipedia gives this:

... This promotes shoot growth, and restricts lateral branching.

The problem is my textbook clearly said that the cytokinin promotes the producing of lateral branching.
Because I couldn't prove the statement and reason, I couldn't give their relationship.
Problem 2
I think even the coleoptile is being cut, the flower must not easy to die. The phytohormone must be related with auxine hormone or other thing.
Because I couldn't prove the statement and reason, I couldn't give their relationship.
Any idea or answer is appreciated!
Feel free to edit my grammar. English is not my native language, but I could understand your post in English.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Why do old willows have so many broken limbs?
Willows have a reputation for being very flexible. In a nearby park (PA), where I often walk, there are about 20 willows growing by a stream. Willows over 30' to 40' tall have almost all their major limbs broken off near the trunk, why is this?
Do willows become brittle as they age?

I took a recent survey:
All willows over about 30" diameter trunk were severely damaged.
Willows up to about 24" diameter trunk showed no damage, even though some are now taller than those older trees.
Those in between showed little damage.
Some of those damaged willows show heavy infestation of wood boring insects on their trunks and damaged limbs.

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. We would need a little more information on these trees - what species of willow are they? I can see 8 species listed for Pennsylvania. Are the breaks recent (i.e. associated with a weather event - storms and droughts can both cause this sort of damage)? Are the breaks all of a similar age or different ages? A picture might help.

@bob1 Thanks for your comment. I added a picture to my question and some other observations. I do not know which species they are, though younger and older trees seem to me to be the same species. The recent heavy wet snow caused one of the infested trees to fall, and large limbs regularly break off during strong winds and storms.

These trees appear to be Salix x fragilis AKA crack willow or brittle willow. The form is more upright and taller than the common weeping willow, but has drooping pendulous thin branches on the lower limbs. We would need to see the leaves for confirmation of species.
These are quite variable in form and are an introduced species in the USA, having origins in Europe and Asia as a cross between two different species, S. alba and S. euxina.
As the name suggests, the tree is fragile and breaks easily from storm, ice, snow etc.  From the common height of break off and similar diameters of the trees, I suspect that they are similar in age and were hit several years ago by a single weather event.
Given your description of the changes in trunk diameter and younger (smaller trunk) trees not showing damage, I would hazard an event probably well over 20 years ago - perhaps the Blizzards of '93 or '96.

so in conclusion, you would say that willow trees do not become more fragile as they age. The group of willow I observed were Salix-x-fragilis "crack willows" which are a very fragile species of willow and most likely were all damaged in a severe storm perhaps 30 years ago.

@Rich Yes, that's about it. I don't think they become more fragile with age, but I guess a young branch might be a bit more flexible so less likely to fracture?


text:
Storage conditions for Propidum Monoazide
I'm a junoir research assistant working on a mini project under my supervisor right now.
I was just wondering if anyone else has worked with Propidium monoazide (PMA) in water for PCR. Currently our protocol is to store our PMA solution at 4°C covered in the dark. However, after reading further literature I have seen PMA after dilution being stored at -20°C or lower, covered and in the dark. I was wondering if there would be any change to the solution between these two methods that would impact my future PCR assessment.
Regards and thank you for taking your time to read this.


text:
How is HIV evolutionarily viable despite its extreme virulence?
How does HIV survive natural selection? And how has it managed to kill far more than any non-airborne virus in recorded history?

Human Immunodeficiency Virus is a mutated form of Simian Immunodeficiency Virus. In simians (Apes and Monkeys, not including humans), SIV is not pathogenic, in most cases, however, when the mutated form made the jump to humans, it became highly contagious and virulent. You can find a basic description in the wikipedia article here: Simian Immunodeficiency virus.
As for your second question, I would likely say that influenza has killed more humans in total than HIV, so you would have to provide a reference for your claim.
However, because HIV is a retrovirus that incorporates into the genome of the immune cells of its host, it can survive in the body for long periods of time in a dormant state. A person may not know they are infected for months or years, and they can pass the virus on to other people. Slow killing viruses such as HIV are very dangerous, as they can be transmitted to large swaths of the population before people are aware they are sick.
Update:
Based on comments, there may be a misunderstanding of the term virulence. From The Karolinska Instetutet medical subject heading (MeSH) definition:

The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.
-The Karolinska Institutet; Virulence

The emphasis is mine, but virulence also refers to the ability of the virus to infect its host, and does not necessary lead to the hosts death. The virus that causes the common cold is highly virulent, but for almost the entire human population it causes nothing more than discomfort.
A virus like Ebola on the other hand is highly virulent in both senses of the term. The reason that there are far fewer cases of Ebola is that it kills the human host so quickly, that an afflicted person will on average only go on to infect about two other individuals, mainly because victims 1) die quickly, 2) are only contagious after symptoms manifest themselves, and 3) requires direct contact with the infected person's bodily fluids.
Contrast that with Influenza which a single person can infect tens to hundreds of people and is contagious before they are displaying symptoms and spreads it with casual contact, or as stated above, with HIV, where a person can be contagious for weeks, months, or even years before they are aware that they are infected, and you see why HIV is very sustainable in the Human population.
HIV also has the added weapon in its arsenal that it can lay dormant in cells for long periods of time so as to escape the detection of the host immune system, and as the disease attacks and kills immune cells, when the dormant virus activates again there are far fewer specialized cells to address the active infection.
Another thing is it is the comorbidity with other diseases that often results in the death of a patient with an HIV infection. AIDS results from other diseases having the opportunity to go unchecked after HIV has decimated the host immune system.

I don't think that answers the question. How is HIV viable? Virulence is selected against.

@Anonstudent - Perhaps you intended something different, but the answer answers the question you asked. Virulence is not always selected against, as shown in the answer.

@Anonstudent You might be thinking of the rate of mortality or pathogenecity (rate an infection causes a disease) -- which also aren't always selected against. There are many niches to fill between the extremes.

@Anonstudent - High pathogenicity is not selected against -- that's a widespread but incorrect belief.  Pathogens are generally selected for transmissibility; in some cases, higher transmissibility is associated with lower mortality, but the reverse is also true in some cases.  Viruses with extremely high mortality rates, like rabies, are perfectly viable on a population basis.

But rabies isn't viable among humans.

@Anonstudent -What's your point? Rabies is viable among dogs and many other species, in which it has a 99.9999% mortality rate.  Viruses like rabbit calicivirus are viable in rabbits in Australia, where there is a 90% mortality rate.  Again, both evolutionary theory, and trivial observations, show that pathogen evolution is linked to transmissibility, not mortality rate.

My point is that, in the long historical term, there aren't any highly virulent viruses that infect humans.

Smallpox was successful in humans and was "highly virulent" by any measure.  You keep making dogmatic claims that are trivially refuted -- you claim that "virulence is selected against", which is false; you claim that virulent viruses don't exist, which rabies disproves; you then claim that there are no virulent viruses in humans, which smallpox disproves.  And, of course, HIV itself disproves all your claims in the first place, for any except the most willfully ignorant denialists.  If you actually have an argument, and not merely a set of constantly-moving goalposts, please make it.


text:
Lyonization in individuals with Turner syndrome
As people with Turner's syndrome have XO chromosomes, does the lyonization of the single X chromosome take place in the somatic cells? Is this one of the reasons for the abnormalities associated with this disorder?


text:
Can someone recommend a recent book on cytoskeletal proteins? Most preferably similar to "Guidebook to the Cytoskeletal and Motor Proteins" from 1998
As in the question, I'm looking for such a book, that will give an overview of the topic from general perspective, with some "branching ideas", and references to literature about them. As for the book I mentioned, I accesed some fragments of it by uni network, and I hope it can serve as a reference of what I'm looking for.


text:
Is Regenerative Brain Tissue Technology In The Near Future?
I got 99% of my information from articles I found in NIH's library; I can't cite anything now because I am on a timed session in a public library.
I've been reading material from research papers in NIH's search engine, I'm no expert in this field but there's this cell called an Embryonic Stem Cell and there are 2 proteins of which I think there could be a probable chance we could utilize them to initiate and halt Stem Cell Differentiation into Neurons and Glial Cells. The 2 proteins are called Fibroblast Growth Factor-2 and Laminin-521, in the NIH article I was reading earlier today it said (paraphrase) that the suppression of FGF-2 expression resulted in ESCs (Embryonic Stem Cells) differentiating into neurons. I also read that FGF-2 maintains the pluripotent nature of stem cells and tends to prevent them from differentiating. I also infer that Laminin-521 could also be important because its important to the health of ESCs.

Laminin 521 Stabilizes the Pluripotency Expression Pattern of Human Embryonic Stem Cells NIH Article

I do not think we are far away from curing things like Alzheimer's or Parkinson's disease, it's possible to reprogram adult cells into Embryonic Stem Cells, that is what the Harvard Stem Cell Institute did.

In order to turn adult cells back into pluripotent or embryonic-like stem cells, scientists use viruses to insert four genes – Sox2, Oct4, Klf4, and cMyc – into the cells.  Harvard Stem Cell Institute

What I am saying is completely hypothetical and speculative but what if we took samples of tissue from other areas of the bodies of patients with nervous system conditions and reprogrammed them back into Embryonic Stem Cells then differentiated them into Neural and Glial Cells to make artificial brain tissue we could somehow transplant into them, or we could somehow get the stem cells to differentiate inside their brains. Anyways the reason I wrote this question is to get a reality check and see how plausible this actually is.

PubMed is an NIH website but things there aren't from the NIH, it's a library site that indexes journals. It would be like saying that Google wrote something because you found the article using Google search, or your local librarian wrote The Adventures of Huckleberry Finn because you checked that book out from the library.

@BryanKrause Oh yeah your right, I'll get that fixed.


text:
Is there a mathematical expression linking effort required to lift a weight and the weight value?
I have no idea if this is the right forum but here we go
I'm basically wondering if there is a math expression linking the amount of effort required to lift a weight at the gym, and the value of the weight
I know there is an expression for work performed
$W = F\Delta d = ma\Delta d$
However, it is linear with respect to mass. If I lift a weight of $x$kg at the gym for 10 reps, and I increase the weight to $10x$kg, I am unable to do even a single rep. So the relationship I am looking for is non-linear with respect to mass.
In essence I want to be able to answer a question of the form:
"I can do 10 reps with $x$ weight, what is the formula to find the weight at which I can do only 5 reps?"

This seems more like a fitness question than a biology one.

I saw this as a kinesiology question... not sure where to post

Pretty sure that Bryan is referring to  our [fitness.se] site, but be sure to take their tour, read their help centre and delete this version here before posting.


text:
Confusion on the definition of time-dependent firing rate and one related formula
(Originally I posted the question on Psychology & Neuroscience SE. But it did not attract much attention. I thought such computational question may fit this site better. Hence I deleted the original post and re-posted it here.)
I am a student majoring in mathematics and would like to further my education in Computational Neuroscience & Psychiatry.
Recently I am reading Dayan and Abbott's Theoretical Neuroscience.
In chapter 1, section 1.2, they defined the time-dependent firing rate as
\begin{equation*}
r(t)=\frac{1}{\Delta t}\int_{t}^{t+\Delta t} d\tau \langle \rho(\tau) \rangle,
\end{equation*}
where $\langle \rho(\tau) \rangle$ is the trial-averaged response function.
And they remarked:

Formally, the limit $\Delta t\to 0$ should be taken on the right side of this expression, but, in extracting a time-dependent firing rate from data, the value of $\Delta t$ must be large enough so there are sufficient numbers of spikes within the interval defining $r(t)$ to obtain a reliable estimate of the average.

The author also said :

If $t$ is small, there will never be more than one spike within the interval between t and $t+\Delta t$ on any given trial. This means that $r(t) \Delta t$ is also the fraction of trials on which a spike occurred between those times.

I want to ask that, what is the exact definition of the time-dependent firing rate $r(t)$?
My understanding is that, $\Delta t$ should be taken such that it is sufficiently small to make at most one spike can happen during $t$ and $t+\Delta t$ for each trial.
Is my understanding correct?

To deal with math in an applied/science field you need to think in terms of reality and practicality and not only in terms of equations and proof.

what is the exact definition of the time-dependent firing rate

This is not really a question that makes much sense. There is no such thing as an exact definition here; the definition is whatever you choose to make it. But we can explain what Dayan and Abbott are talking about.
Let's think about what it means to have a time-dependent firing rate, physically. "Firing" is a discrete event, occurring at a moment of time with arbitrary precision. A firing rate is a probability, or more specifically a probability density, for that discrete event to occur.
There is no underlying reason for a probability density to itself be discrete, it can change at arbitrary time. That's why Dayan and Abbott write that the dT might as well be taken to the limit of zero. But we also expect probability densities for spikes to be relatively smooth, so there's not much lost if you use dT that is small but doesn't approach zero. So, practically, discrete is okay.
There's also not much need for spike times to actually be tracked with arbitrary precision. Spikes will result ultimately in current flowing through channels into cells; cell membranes are capacitors with some time constant. If you're trying to model the effects of a spike, you're not going to be able to really tell the difference between time differences that are much smaller than those associated time constants. So again, practically, discrete is okay.
Finally, let's think about actual measurement and estimation. That's the motivation that Dayan and Abbott actually raise. If you want to estimate a firing rate from actual spike trains from actual data, you're going to have a finite number of events all at arbitrarily precise times. The first place you're going to lose the actual arbitraryness is going to be at the sampling rate of your recording equipment, so there's that. But even if that's not an issue, what happens to your estimated probability density as you get to smaller and smaller dT? You're going to end up with an estimate that is either 0, because you never ever observed a spike in that bin, or 1/nTrials. This isn't very helpful. I mean, it represents the data accurately, but it doesn't tell you anything. Much like you might summarize a sample of heights with a mean and standard deviation, the whole point of expressing some statistical quantity like firing rate is to be able to generalize and predict. So, it doesn't make sense to express firing rates based on data at a higher time resolution than we have actual data available to make a representation.
An alternative to Dayan and Abbott's approach of not letting dT be too small would be to convolve the discrete spike train with some smoothing kernel like a Gaussian. But to represent these things in a computer we're going to eventually end up with something discrete at some level.
For some cases, you might want to ensure a spike train is binary per trial for a choice of dT, but I wouldn't say it's necessary per se.  A reasonable choice of dT will depend on the specific system you're modeling and what you're doing with it. For many computational tasks you'll also be dealing with computational constraints that may make a finer time resolution expensive to deal with while not providing an appreciably different result.


text:
Correct migration rate expression in infinite island model
In Sewall Wright's infinite island model, where all demes exchange migrants each generation, I have seen the migration rate stated variously as $m$ or $\frac{m}{d - 1}$ (as in Matthew B. Hamilton's Population Genetics textbook, chapter 4, p. 132, figure 4.12), where d is the number of demes.
My question is, which expression for the migration rate is the correct one?
If it's the latter, then where does the "-1" come from?

Definition of $m$
There is no correct or wrong expression. It all depends what exactly you are interested in and what is the definition of m in a specific paper.
Def. 1
Some models assume that $m$ is the migration rate from a given population to another given population.
Def. 2
Some models assume that $m$ is the probability of migrating to any other population. In a two population case, this definition and the above are the same. In other case, the probability of migration to a given population is $\frac{m}{d-1}$
Def. 3
Some models assume a migration pool. With probability $m$ an individual is a migrant, goes to the migrant-pool and is then redistributed among all other populations (only works for island models). In such model, a migrant could be an individual that actually come back to the same population. So, the probability of really migrating is $\frac{m (d-1)}{d}$ and assuming equal migration rate among all populations, the probability to migrate to a given population is $\frac{m}{d-1}$.
Fst
If you're dealing with $F_{ST}$ in a finite island model, then you will have some $\frac{m d}{d-1}$ terms. I talk about it in this post but it is not complete, so you might want to read Slatkin (1991) and Charlesworth (1998)

Thanks! Though this is a bit more challenging. I am building an R simulation where I have $K$ subpopulations and a migration rate of individuals. Initially, I just set the migration rate equal to $m$ (or $\frac{m}{2}$ for Kimura's linear stepping-stone model), but now I see that it should also depend on $K$.

Well, it depends upon what definition you want to give to $m$. If you want to match your simulations with results of some other paper, then make sure to copy their definition of $m$. Otherwise, most people call $m$ as being the migration rate between any two populations (without migrant pool complication or anything). Note however, that if you have populations of different sizes (or if migration depends upon local population mean fitness aka. hard selection), then the forward and backward mutation rates may differ and you'll have to make your definition clear regarding this issue again.

R is extremely slow. You'll find plenty of simulation platforms written in C++ that will be infinitely faster that what you'll code in R. So, if you need speed,
you will find advice here. SimBit is a simulation platform I wrote myself if you are interested.

Thanks! I will take a look at SimBit. It sounds very interesting.

Do you know where the -1 in the equation for the migration probability comes from? My guess is that it is used as a correction factor to make the estimator unbiased, but I am uncertain.


text:
I have brown tiny bugs all over the house
These bugs are crawling all around in my house, firstly they suddenly appeared in the kitchen after the 2-3 days of continuous rain. but then it started to move on sofa, bed, all on clothes, they move very slow and dont fly but dont know they somehow moved to worn clothes and transferred to other parts in house. and also they bites which is more irritating
i am unable to get more pictures clearly its very small.

this is the closest pic i could manage to get clearly
i did pest control in house but there was no effect on them.
some how after few days we mopped whole house and furniture with harpic's acid based Clear after that we didn't se them for 3-4 days but again it came back.
even person who did pest control he said there is no description in their directory of this bug.. please if anyone know or faced  issues about this bug please help with the suggestion on how to terminate it.

I'm guessing you are from India based on your name. Is this also where you are in the world? ID for insects is quite regional, so a location is important. Dimensions would also help.

yes i am from Pune, Maharashtra, India. currently raining season is here.


text:
What is the ploidy of endosperm formed through apomixis
From my limited knowledge, apomixis there is no fertilization. And there is no meiosis either.
So how does the mechanism for this come about and how can we find out the ploidy of the endosperm formed?
The example we got in the text is when a diploid egg cell without meiosis becomes a seed (if that helps).
Are there other kinds of apomixis present?


text:
Do these pictures of human gestational sacs include embryos, and, if so, where?
This article in the Guardian, What a pregnancy actually looks like before 10 weeks – in pictures, includes a number of pictures of human gestational sacs.  The article seems to imply that each picture "includes the nascent embryo", but I'm puzzled because I think that the embryo should be visible in these pictures, yet it is not.  For example, the seventh picture in the article shows a gestational sac removed after eight weeks of pregnancy.  I believe this is a gestational age, measured from the last menstrual period, so according to this embryological info the embryo should be 8-11 mm long, and easily visible, given the scale of the pictures.  However, I don't see it at all.  Has the embryo been removed, or do these pictures include it, and if so, where?  You can also see these pictures here and here.  You can see some pictures of early embryos here.

Yes, it is visible, just mostly translucent.

The article also specifically says  hard to see: "This image shows the gestational sac of a nine-week pregnancy. This is everything that would be removed during an abortion and includes the nascent embryo, which is not easily discernible to the naked eye".

I can't point to a quantification, but I'd expect the embryo to be no more vascularized than any of the supporting tissue around it. I have much more experience (not much, just much more..) looking at other developing organisms at similar size and...yeah, they're pretty hard to see unless you have a stained histological specimen or something.


text:
Is the vibration from my fridge enough to harm my aquarium?
I keep a small snail aquarium on top of my dormitory fridge. Recently, someone suggested that this setup is unethical because the fridge's vibrations might disturb the water and stress the snails. However, the aquarium is placed on a thick rug for cushioning.
The tank is equipped with a large air pump and sponge filter, as well as a decent-sized internal filter. Both of these create significantly more water movement than the minimal vibrations from the fridge.
How exactly could my fridge harm my aquatic life? Does this concern only apply to louder or older refrigerators?

Edit:
I have been asked to show previous research. This is a bit difficult to do, as my previous research failed to answer my question (hence why I am here).
But perhaps these will help:

https://www.redditmedia.com/r/AskEngineers/comments/1hd7m1k/what_can_i_place_between_my_fish_tank_and_mini/

I hit a wall at showing the vibrations from the fridge were strong enough to cause water changes or that they were any different from the water change supported by the air pump and filters.

I've often wondered that about aquarium air-pumps too. Please take our [tour] and refer to the [ask] section of the [help], you should then [edit] to add some evidence of your own researches into the topic, your attempt to find an answer and where you hit a wall- we encourage that here.

Note: there is a [pets.se] site on the network that might be of interest to you.

Finding specifics for your model/age of fridge is asking a bit much of humble researchers to have gotten funding to support the study in the first place. For a more complete answer, I seriously doubt anyone's done research that specific. However, bit of judicious poking gave this: Noise and Muscles but that's another mollusk entirely. (Frankly, it's not unreasonable to generalize a little IMHO).


text:
How long can the brain survive during ongoing cardiac arrest?
There was this interesting discussion on CPR and defib in response to the question "Why can't we defibrillate the heart within 1 minute after ventricular fibrillation by electroshock?".
Now I was wondering "How long can the brain cope without O2?".
And to specify this question to a realistic situation: "How long can the brain survive a cardiac arrest without (gross) neurological symptomatic consequences?"
I would define "gross symptomatic consequences" as "noticeable and debilitating" in one way or another to the subject. This opposed to minute changes in, e.g., motor response latencies measured in a laboratory task designed to pick up the slightest results of asphyxia.
As background: I did these CPR and defib courses and the first thing they tell you to do is (1) call 911 / 000 whatever alarm number and (2) arrange a partner in crime to help with CPR;  or in case of a defib situation, (call alarm nr), make your way to the defib, unpack, apply electrodes, look at the manual, casually wait for instructions/warning lights etc. But..but... there is a person here without oxygen supply to his brain! And I know professional staff should be brought to the scene, but what struck me most is that starting up the defib (which inherently takes time) is more important than CPR (which is immediate)? In other words, loosing precious minutes is advantageous over diving straight away into CPR and pumping blood around?

Fibrillation is very hard to detect clinically. It can be confirmed only on ecg (as far as my knowledge extends). So unless the patient is at high risk of fibrillation, generally cpr is the first aid done

From Boron and Boulpaep textbook of Medical Physiology, second edition, p.289:

Because of falling ATP levels in the brain, consciousness is lost within 10 seconds of a blockade in cerebral blood flow. Irreversible nerve cell injury can occur after only 5 minutes of interrupted blood flow.

If conscious is lost within 10 seconds of blockade in cerebral blood flow, I guess a person will not be conscious to do any action in only 10 seconds!
Brain ischemia is divided into

Focal ischemia which signifies stroke.
Global ischemia which occurs in cardiac arrest.

Permanent neural injury means that once perfusion is restored, the symptoms don't relieve as the part of brain which caused those symptoms becomes dead irreversibly.
For a list of symptoms check this page.

If we consider another case, there is blood flow, but no new oxygen is coming into the system, the brain cells may begin to die after about four minutes [1]. However, this depends on the person not the amount of time. Consider free divers and more specifically Tom Sietas. These men and women, in this sport, can go well beyond the 5 minute mark with no debilitating brain damage. Now, Tom Sietas holds the world record for static apnea with the time of 22mins and 22sec under water without air and yes he survived. Here is a news article about Tom but it goes on to say Pearl divers go about 7mins without air.

@ChrisStronks I would guess, with these people (free divers), since their body is trained, they could go into cardic arrest and last longer than 5 mins but this isn't a testable scenario.

Interesting answer, +1. However, I think we are indeed talking about exceptional, trained cases here, which would make an interesting new question as to how they exactly cope!

@ChrisStronks I know they are exceptions but we can't say 4-5mins is a hard limit. It all depends on the person. In the case of Tom, I could die four times before him.

I think such training will enable the lungs to retain more oxygen (well developed lungs that expand fully) and the circulatory system is better adapted by increasing hemoglobin concentration (this increases the blood carrying capacity). It has nothing to do with cerebral perfusion. Cut blood supply to brain no one can stop symptoms from occurring.

@CRags I said let's consider a case with blood flow and no new oxygen.


text:
Are bears related to dogs in a similar way to how cats are related to 'panthers'?
I've tried searching on Wikipedia but I couldn't find what family dogs belonged to. Ursidae is 'bears' and Canis is 'dogs' ; Panthera is big cats like:- tigers and jaguars is what I know.

You will be interested int he ressources from the post The best free and most up to date phylogenetic tree on the internet?

No, because panthers are cats, but bears are not dogs. You can see their phylogeny in a figure from one of my papers here: https://www.researchgate.net/figure/Most-likely-phylogram-derived-from-the-Bayesian-Analysis-ln-533753675-Numerals_fig1_6550244
As you can see, Bears are most closely related to pinneped (seals and sea lions), with dogs as sister to that group.