text:
How to find out what biological effects a molecule has, without having a specific mechanism or pathway in mind?
I'm interested in finding what biological effects a (small) molecule has in a high-throughput and "low-assumption" way. I'm mainly interested in cell-based assays.
Background: There are easy/fast assays of high level phenotype effects eg cell proliferation or differentiation, but those wouldn't pick up lots of molecules as being active at all, unless they're at toxic levels. There are also a lot of assays which look at a specific pathway, eg using a Western blot with an antibody to a phosphorylated protein (phospho-Akt comes to mind). But those don't help if one doesn't already know the relevant pathways; they're more useful if screening molecules that target a known pathway, or confirming a known/suspected mechanism of action (and also most really aren't high throughput).
I'm interested in assays which can produce information on everything a molecule does when interacting with a cell, if possible in a single experiment.
Some things that come to mind:

Gene expression profiling (eg using microarrays or RNAseq): gives information on the expression of everything; it is comprehensive and reasonably high throughput. The main limitation is that expression is usually a few steps downstream of what the molecule would interact with, unless it is literally interacting with transcription factors; so it would usually require tracing changes back up various signalling pathways
Proteomics (eg 2D-PAGE, shotgun proteomics): gives information on protein abundance, and potentially post-translational modifications. Seems hard; for 2D-PAGE for example typically a couple of thousands of spots can be identified (a fraction of the whole proteome), and the amount of protein in each measured to within ~20% accuracy (semi-quantitative). Possibly also needs a fairly large sample
Metabolomics (eg LCMS): gives information on all metabolites

Are there any other types of assays that would give information across all/many genes/proteins/enzymes/signalling pathways?

Okay, I cleared up the comments here including my own. You're right, they're unfriendly. But, on the other hand, your question is pretty rude, too. You're asking for a shortcut to knowing everything, seemingly without having done any work yet yourself. It does sound like you're looking for something very similar to a company recently in the news as a scam. Why do you think there is some magic secret method you can learn by asking a single question on Stack Exchange while everyone else in biology is working hard on other methods? Do you think they're just wasting their time and money?

You're also dismissing techniques that other people put a ton of effort into developing because they're "too hard". Science isn't easy. Everything easy is already done, hard is all that is left. If it's easy, it's not valuable.

@BryanKrause I'm sorry it came off that way. I am actually very familiar with the opposite problem: given a target protein/pathway, find small molecules/peptides/proteins that interact with it. It seems most biochemical and cell based assays are optimized for that, while finding all things that a specific single small molecule interacts with is a much less common type of screen. Possibly it's just my unfamiliarity with that type of workflow, but the answer is highly non-obvious. I don't expect a secret method, and I'm not dismissing methods which are hard, just noting that

Personally I think this is a poor question, because the answer is immediately obvious to anyone who was worked with current technologies for both proteins and nucleic acids, but as always, it is hard to prove a negative.
The short answer is NO, not even close to a single experiment or assay that can tell us EVERYTHING  a single protein can do/interact with. If there were, we would be in a situation where almost all of cell biology could be done in a few thousand experiments.
Let's take a well known protein that people have been studying for quite some time now - the "Guardian of the Genome", Tumour Protein p53 (TP53, AKA p53). This is admittedly an integral protein to cellular function, so has a lot of interactions - but it serves to illustrate the point.
Now, let's head to the STRING database for this protein. STRING is a database that charts protein-protein interactions through a number of sources, mostly from the literature, but also through predicted interactions, with varying levels of confidence. Check out the legend and settings tabs for the page to see how those work.
The initial page for p53 should show you p53 and 10 other interacting proteins - these are the most highly significant interactions, with the greatest confidence in them being real. Now, click on the "+More" tab, and you should see 20 interactions - do this a few more times and watch that number and the complexity of interactions grow - it'll show interactions, not just with p53 but between other displayed proteins too. This is a fairly simplistic way to show the number of interactions a single protein has inside the cell. You should finally come up with a few hundred different proteins that have been found to interact with p53. Now, don't forget these are protein-protein interactions only.
p53 is also a DNA binding protein - it is predicted to interact with the genome at about 55,000 binding sites (see sect 2.1, para 2 in this publication) - What does it do at each of those sites? Short answer is - we don't know. Maybe upregulates something, maybe downregulates, maybe nothing, maybe something else.
There's also some evidence that p53 interacts with various types of RNA molecules, some of which are only relatively recently discovered, so assays for them are still fairly primitive. Again, what it does there, we don't know.
If you have ever worked with proteins and DNA, you will know that the methods of working with each are usually quite distinct - which also puts a technological barrier to your idea of a single unified assay. Of course, it is entirely possible to do DNA or RNA-protein interaction studies (e.g. ChIP), but to do these at the same time as protein-protein in a single assay - no chance.
There's also a second (third?) problem - sensitivity. Currently, with most technologies, you can have it one of two ways, but generally not both! You can either detect the rare interactions - the 1 in 1,000,000, by removing the common ones; or you can see the common ones but not the rare, because the common ones swamp the rare. An example of this is in RNA sequencing. In a cell, ribosomal RNAs (rRNA) make up about 80% of cellular RNA, despite not coding for proteins (that I know of). So, if you want to look at a cellular coding RNA by next-gen sequencing, most of the time you will do a rRNA depletion or else 80% of the raw signals will be rRNA, which is a waste of your useful information achievable.
Edited to add:
As has been clarified in comments, OP is not asking for a single assay to do all, but rather types of assays that might be suitable to produce similar results - basically things like Next Gen sequencing, but for small-molecule (not necessarily protein-protein) interactions, which essentially turns this into a shopping question, which are generally not considered appropriate for this site as tools/techniques change quite frequently. It might be more appropriate on bioinformatics.
As always, the content I wrote above applies, particularly the bits about sensitivity and technological barriers.
As far as I know, no such assays exist for proteins, but the one that might come the closest is protein mass spectrometry by MALDI-ToF with de-novo peptide sequencing. These are (in my very limited experience with them) by no means as trivial as setting up a Next Gen sequencing run, but I am sure the technology and associated bioinformatics tools will improve and mature over the next few years.

Thanks for the answer; I'm sorry you think it's a poor question, let me know how it can be improved.  I'm looking mainly for a way to find what external treatments interact with; small molecules which act on surface receptors or diffuse inside the cell, rather than interactions of proteins already in the cell. STING is a cool database! I looked at the type of experiments used to build it, a lot of it is either co-immunoprecipitation or affinity chromatography. These are specific to PPI, again very cool but don't work for the small molecule scenario

"a single unified assay" - I mean a single assay per type of result, not single unified assay for everything, of course. For example all proteins a small molecule binds to, or all changes in phosphorylation due to treatment with a small molecule. Roughly in the way that RNA-Seq gives information on all RNA, whereas RT-qPCR only looks at one or a few selected ones.

@AlexI so I'm interested in assays which can produce information on everything a molecule does when interacting with a cell, if possible in a single experiment. doesn't mean a single assay - 'cause that's sure what it reads like to me. You've improved the question, but the complexity of the problem still stands. PPI like with p53 is a single example. Yes, there are mass methods - next gen sequencing is great for genomic and RNA effects, but nothing even remotely similar exists in the protein world that I am aware of.

@AlexI - I also read your question as one assay to determine everything, etc. which, I confess, was the reason for my downvote. That is in reality a preposterous request. If you actually meant something different, it didn't read that way.

@anongoodnurse Yeah, what I meant was one molecule x a view across all targets/pathways/etc, rather than the more usual screen of thousands of molecules x one target. The examples hopefully clarify that, RNA-Seq is an example that works to quantify the effects on the transcription of everything at the same time. I was looking for methods which provide similarly comprehensive data on (eg) binding, phosphorylation, etc. Please feel free to add an answer if you can think of anything.


text:
Is continuous exposure to blue light lethal for mosquito larvae?
I have been observing developing mosquito larvae since 2 days and I saw, while exposing my laser light of blue colour to it, that it becomes unstable on exposure to blue light.
Thus, I wish to ask, will it die or whether it is fine? It has been one day since I shone the light on it, so please tell me: will it grow further or not?

There are lots of relevant results from Google Search for "blue light mosquito larvae". Here is just one of them:
https://www.nature.com/articles/s41598-022-14096-y
They are not all only mosquito related either, such as this one for insects in general:
https://www.nature.com/articles/srep07383
Or you could just find out for yourself. You are already set up for it. All you need is a control group, and preferably a third group that is exposed to high intensity laser light of a significantly different wavelength such as red or green in order to determine if it is just the intensity of the light or the wavelength.

source: Stack Exchange

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

sort: votes


text:
Movement of the Ribcage during movements of the Thoracic Spine
I want to find a rough relation between the angle of rotation of the thoracic spine and the corresponding segmental movements in the skeleton of the ribcage. I have come across some research which explains in detail the anatomy and axes of rotation for costovertebral and costotransverse joints.
I have also come across literature providing the movements of ribcage in the case of inhalation/exhalation.
However, I haven't found any literature that details the overall/partial movement of the thoracic wall or ribcage bones during thoracic movements. (flexion, side bending, axial rotation etc.) There is also a previously asked unanswered question regarding this topic.
Can anyone suggest any previous work/paper/book/website that can provide me with a detailed kinematics of the thorax region?
Also, can the rotation/translation of ribcage bones be approximated if I know the angle and the axis of rotation of each thoracic vertebrae?

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


text:
Calculation of blood flow rate and pressure change in heart
Question: Blood flows from the left ventricle of the heart through the aortic valve and then to the aorta for system circulation. In a patient, the diameter of left ventricle outflow tract (LVOT) is found to be 1.6 cm, the aortic valve 8.0 mm and the aorta was 2.0 cm. Vitals of the patient indicate a 5.0 L/min cardiac output, a heart rate of 70 beats per minute and a duration of the ejection phase during each beat of 300 ms.

What is the volumetric flow rate during the ejection phase of the beat?
What is the pressure change over the valve?

You can assume the density of blood to be 1.06 g/cm3.
(answers: $Q$ = 0.24 L/s, $Δp31$ = -440 Pa)
For the first question, I tried to use the formula:
$Q = AV$
Where $Q$ = Flow rate, $A$ = cross-sectional area, and $V$ = velocity.
I calculated $A$ for LVOT, valve, aorta with $\pi r^2$, and calculated $V$ by dividing the diameter with 300 ms, and calculated $Q$ (with unit of L/s) by $AV$. Then I calculated the volumetric flow by adding each flow rate, but the result wasn't 0.24 L/s. I guess my approach is mistake, but I don't know how to solve it then.
For the second question, with bernoulli's equation, I tried to calculate the pressure change by $(0.5)*density*((V $of lvot$)^2-(V $of aorta$)^2)$, but the result wasn't -440 Pa. What are other things I should consider?

Is this possibly better suited for medical sciences? The question can be migrated if you want.

It's more of just a physics question; no biology or medicine is needed to answer.


text:
What are possible tweaks when a protein expression from a plasmid shipped on paper fails?
In my group we recently tried to express a protein necessary to perform an analytical method in BL21(DE3). The first two attempts did fail and no colonies did grow on the agarose. I hear, that the extraction of plasmid from paper and resoubilization is more prone to error in comparison to plasmid that is shipped in liquid form and this is a known issue. I am wondering what could be possible workarounds to try to still get it working. Until know, I have the following ideas:

Increase plasmid concentration
Decrease antibiotic concentration
Use a different strain like NEB 5 alpha

I am also wondering if the X-Ray treatment of customes service could facilitate in any way plasmid determination or is this an urban myth?

How did you prepare the plasmid from the paper? Did you do a transformation and a mini prep first?

No miniprep. I took the sheet of paper and cut it leaving a small portion as backup. Solubilzed the plasmid with 50 microliter TE buffer, resulting in a plasmid concentration of 11 ng/ml. Using 4 microliter plasmid with 25 microliter bacteria culture. Did not work. Than increased to 10 microliter plasmid, did not work. I observed now increased plasmid concentration of ca. 17 ng/ml after adding 100 DNSase free water destilled water and letting it stand over night.

Ok: My advice in these cases would be to first transform some standard competent cells (DH5a or likewise), cultivate them, make a prep and check your plasmid at least on a gel, ideally but restriction digest. Also make some glycerol stocks. So you make sure you have the right plasmid and you have a stock you can always go back to.

I will consider this after my current experiment batch. I will do 5 plates, 2 with Ecoli 21D3 and two with NEB5 alpha, two different antibiotic concentration and 1 plate just with LB media at the smaller antibiotic concentration. Therefore I should be able to reduce the amount of possible error sources based on the outcome of the experiment. When not a single of 4 plates show colonies I agree, the integrity of the plasmid is in doubt.

I think that your title here is entirely misleading - you aren't looking at protein expression in this case, simply transformation of the bacteria with a plasmid. Frist step is to test that your system works with your cells and plasmid and with known good cells and plasmid - beg/borrow known good competent cells and plasmid from a colleague and test them in parallel with your cells and plasmid. Note that you need competent cells for this, not just bacterial culture.

You're right. Goal is of course the expression after the trafo. Cells are competent. In the meantime I also got colonies and we will do a miniprep and check the plasmid.

In my case it helped to treat the filterpaper longer with miliq water to increase plasmid concentration. I also used more plasmid in the 3rd attempt and it worked. Miniprep was performed nevertheless. When a similar experiment is not working, I would recommend to increase plasmid concentration, increase incubation time and decrease antibiotics in that order. I tested the plasmid on agarose gel and further I sent the plasmid further to a sequencing service for validation. Seems all to checkout.


text:
How to elute the protein that is bound to biotinylated RNA immobilized with streptavidin?
I would like to test the proteins that bind to biotinylated-RNA by mass spectrometry , I was using Dynabeads™ MyOne™ Streptavidin C1 (invitrogen) coupled with biotinylated-RNA,than mix these beads up with cell lysate to achieve protein-RNA interacted solution, so does anybody know the better idea to elute that protein out of the mixed reagent?

What does the manual say about elution?

It doesn't have any info about elution

If your end goal is mass spec, you could do an on-bead digestion of the protein. Alternatively you could elute the protein with SDS buffer and do the digest in a gel. It should also be possible to break the protein-RNA interaction (eg with salt, cosolvents, and/or pH)

any specific protocol or detail with it?


text:
Looking for a recommendation: Anatomical diagrams of animals commonly used in laboratory testing (potential surgical procedure emphasized)
I'm interested in either a book or a place to find well-drawn diagrams of animal anatomy. The emphasis if possible would be on anything which includes material related to the nervous system of neurosurgical procedure. I'm interested in diagrams or figures for animals commonly used in testing, that is mice, rats, or others. This would be similar to the diagrams shown in medical school. I'm interested in these from the perspective of someone doing surgical procedure on a testing specimen. Any recommendations (book or otherwise) would be greatly appreciated.
Also, if there is a better stack exchange site that you would recommend me asking this on, feel free to recommend and I can move my question there. I'm outside of either field (engineer), so apologies if I'm, not familiar with which subforum to ask this on, and let me know where to move the question.

You'll probably get a better answer if you are more specific about the procedure of interest.

Neurosurgery was given as area of interest. Procedure of interest would involve operations on the central nervous system (CNS) and peripheral nervous system, particularly that of the spinal cord. Interpretation of spectral frequencies/brain waves of specimen is also of interest. I'm in the early phase of planning so anything even tangential to this would still be valued.

Neurosurgery is very broad though; you could be looking for brain atlases or neurovasculature or peripheral nerves. And now you bring up spectral analyses? You really need to have more focus before asking a question here, it's like if you asked for a book on engineering and said you're interested in electrical and mechanical and industrial, while architecture and geology are also of interest as is anything tangential.


text:
Movement of solutes across a semipermeable membrane in a U-shaped tube

The solutions in the two arms of this U-tube are separated by a membrane that is permeable to water and glucose but not sucrose. Side A is half-filled with a solution of 2 M sucrose and 1 M glucose. Side b is half-filled with 1 M sucrose and 2 M glucose. Initially, the liquid levels on both sides are equal.
When it reaches equilibrium, the sugar concentrations on both sides of the U-tube will be 1.5 M sucrose and 1.5 M glucose.
Can somebody explain the answer (D) to me? My understanding is that the membrane is permeable to glucose, therefore glucose will reach equilibrium, with 1.5M on each side. Since the membrane is not permeable to sucrose, the concentration of sucrose will not change. Water will move from B to A. Does the movement of water causes the sucrose solution on both sides to be equal? But wouldn't that alter the glucose concentrations too? I'm sorry I just know what my bio teacher told me but I don't quite get the reasoning. Thanks.

Please do not post questions as graphics. They do not index and discriminate against people with visual impairments.

OK I'll modify it

The membrane allows movement of particles which will cause a balancing of the concentrations.
There is one hint in the text: "Initially, the liquid levels on both sides are equal" which gives away how this will happen.
Water and glucose can freely move through the membrane and this is what will happen. Water will move through the membrane, the level in side A will rise until both concentrations of sucrose are equivalent. Glucose will also cross the membrane from B to A until the concentration is equal on both sides.
You are right, the movement of water will lower the concentration of glucose in side A but since the glucose can move across the membrane as well, this will not affect the equilibrium.


text:
What is this cocoon (if that is what it is)?
I found this cocoon (or what I think looks like a cocoon) in an urban hedgerow in Upper Bavaria, Germany in early October (begin of autumn).
Around was a web, but no inhabitants were there.
Its diameter was about 3 cm and its opening showed towards the sky.
Thank you already for hints! :)

I guess, I figured it out: it seems to be an abandoned cocoon of a wasp spider (Argiope bruennichi).
Images for comparison are found on Wikimedia Commons and on iNaturalist.
Only thing that puzzles me is that usually the spiderlings overwinter in the closed cocoon and it was opened already in autumn (and the hedgerow is - unfortunately - neatly cut each autumn, so it is impossible the cocoon was there since the last year).
Anyway, I guess someone might have preyed on them... ¯_(ツ)_/¯


text:
Storing bacteria in a dry, room temperature long-term storage whilst maintaining viability
I'm quite new to biology, but I'm wondering if there are any methods of storing bacteria in long-term, dry conditions with no climate control. Perhaps they could be dormant in a powder or granule-like form similar to yeast. The species that I'm trying to work with is a gram-negative bacteria called C. Metallidurans. What's pretty cool about this bacteria is its ability to survive in environments that are high in heavy metals and produce pure gold from gold chloride. Any advice helps, thank you.

Lyophilization, aka freeze-drying, is probably the go-to method of microbial preservation without the need for cold storage. It's how bacterial strains purchased from commercial culture collections are typically shipped.
The process consists of first freezing cultures in a lyophilization buffer containing a mixture of cryoprotectant and lyoprotectant excipients, which is exposed to a strong vacuum (while maintaining sub-freezing temperatures) to sublimate the frozen water out of the mixture (source). The lyophilized powder is typically sealed in a glass ampoule filled with inert gas for long-term storage, but can also be packaged in any number of ways to for application-specific uses.
Unfortunately, there's probably not a one-size-fits-all formula that works best for every organisms, but there may be some approaches that are "good enough" for most. Under the right conditions, lyophilized cultures can be stable for years with minimal loss of viability, but I wouldn't count on it without extensive optimization and process validation. Also would not recommend it as your sole method of long-term preservation. Best practice is to always keep glycerol stock backups at -70°C or colder, and to have a plan in place for how often these stocks should be assessed/renewed.

Nice answer. I'd add that it needs some specialist equipment to freeze dry under the controlled conditions needed.

The answer to this strongly depends on the species of bacterium you are working with.
The only ones that I know of that are capable of withstanding any dehydration process are those that form spores. The spores are tough, long-lasting structures that enable the bacterial species to resist environmental changes.
Cupravidus metallidurans, the species you are working on is not a spore-former, so it isn't possible to fully dehydrate them. However, it is possible to form long-term stocks of many, if not all, bacterial species in glycerol and frozen at -80 C (ultra-cold freezer) sort of temperatures.

Most bacteria can tolerate lyophilization under controlled conditions, which essentially results in a desiccated powder. But it's a highly controlled process and the long-term stability of freeze-dried bacteria is more variable than that of frozen glycerol stocks.

@MikeyC true - I completely forgot about freeze drying. I was about to suggest you write it up as an answer, but then saw that you already had.


text:
max % of oxygen not harmful for breathing?

Is breathing pure oxygen bad for you?
Human blood is designed to capture oxygen and safely bind it to a molecule known as hemoglobin. However, if you breathe in a high concentration of oxygen, it will overwhelm the blood, disrupting the central nervous system, damaging the lungs, heart and brain.

Breathing 100% oxygen is harmful for the lungs and the brain and will cause death  under normal pressures.
link
Continuous exposure to oxygen under normal pressure leads to death , however exposure for limited amount of time or under low pressures delays death or damage to organs
The Earth's atmoshphere has around 22% oxygen.How much is the upper limit of % oxygen before it becomes harmful(death or damage to organs) to a human?

Oxygen is also harmful at 22%; like most poisons, there isn't some magic threshold at which harm begins, though you can define one and go from there. How would you like to define the threshold at which you will start calling it harmful?

@BryanKrause If it were harmful , wouldnt we be not able to live on?

We can't live forever on it, over time it causes us heart and vascular disease, cancer, etc. In the shorter term, it contributes to us needing to constantly replace proteins and other cellular components. It also almost caused the extinction of all life on earth, before life had evolved to deal with it. https://en.m.wikipedia.org/wiki/Great_Oxidation_Event

We need proteins regardless of this to feed the muscles off.And if im not mistaken , cancer doesnt come out in every human.

Muscles do not feed off protein typically, carbohydrates are the energy source. Protein is needed in diet for amino acids which build proteins, including in muscle. Cancer is sort of a chance game; things that cause cancer create more opportunities to "win" that game through damage to DNA, it is not deterministic. There is lots of DNA to potentially damage; cancer happens when the damage happens to occur in the right combination of places

You stated that at some percentage O2, be would not be able to keep on living. How are you defining death caused by O2 in excess of 22%? Are you only considering lung damage?  Must the death be acute or is chronic oxygen toxicity causing death acceptable? I know it sounds strange, but I think you need to put some kind of parameter on death by excess O2.

As a new user to SE Biology please complete the [Tour] to find out how this site works (we know you haven't as you don't have the badge). This is a site for students and professionals in Biology and posters are expected to show that they have conducted some research on the topic. Please help us to maintain our standards.

@David Been editted.

Oxygen is always harmful.  It's tearing apart your cells as we speak.  That's actually what we like about it.  It's really good at tearing apart food molecules to get at the juicy energy inside, but it will also tear apart other things in the process.  Oxygen and the oxidizing effects of it are probably a major factor in aging.  When it first appeared on the planet in any sort of concentration as a waste product of photosynthesis, it led to the world's first mass extinction event.  Since then, animals have evolved to not only tolerate it, but require it.  Doesn't mean it's not still tearing you up from the inside though.  The concentrations present in the atmosphere are the concentrations our body has become adapted to cleaning up after.  Unless you need higher concentrations for some medical reason, stick to atmospheric concentrations.

As I'm sure you know by now, this site likes objective answers that can be backed up by references. Please edit your answer with suitable references for your claims.


text:
Can a gene transfer from a plasmid to a bacterial chromosome?
Plasmids are involved in providing resistance to antibiotics. So, can that gene or any other gene transfer from the plasmid to the bacterial chromosome?
Is there any chance where antibiotic resistance is conferred by chromosomal DNA (not plasmid DNA)?

Briefly: yes.
It has been known for some decades that plasmids (including those that encode antibiotic resistance) can recombine with the host genome.
Indeed, the selective pressure to perform such transfers makes it possibly more interesting to infer why it doesn't happen (in appropriate contexts), for example in this paper.


text:
What's the difference between a transformant and a recombinant dna? And how to differentiate them both?
I'm unable to understand the difference between the both. Would be really grateful if someone can explain it to me, in simple terms..

Can you show us the text that you find confusing? One normally thinks of a transformant as a clone of cells that have been transformed with some transferable DNA such as a plasmid (which could be a recombinant DNA element). But I think you could have found that with a simple google search.


text:
centrioles in primitive plants, algae and fungi
Do these groups of organizms lack centrioles or possess?

Red algae (yes?)
Diatoms (no?)
Yest (no?)
Chydtridiomycetes (no?)
Liverworths (yes?)
Hornwoths (yes?)
7.Zygomycetes (no?)
Cannot find exact answers, complicated case. Need help.

this may get closed for being more than one question but until then , yes for hornworts. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240993/


text:
What type of tortoise is this?
Found him on the street in San Antonio subdivision unsure of what type of tortoise he might be.

A photo of the underside and hind legs would be most helpful for precise ID. From the location and limited visual, it looks like a young Texas Tortoise which is an endangered species. Very cute!


text:
Chloroplast arrangement in high and low intensity of light
I have read that there are different alignments of chloroplast according to the intensity of light.
I read that in high intensity the chloroplast align themselves parallel to the incident light (Parastrophe).
While in low intensity they align themselves perpendicular to the incident light(Epistrophe).
But somewhere else I read that they align  perpendicular to the light in high intensity while parallel in low intensity.
So I'm confused which information is true...can u please tell me which one is correct?

Where did you read this?

Well....I read the first one in a book....and the second one on Google....and now I'm confused which fact is true....at high intensity, do chloroplast align themselves parallel or perpendicular to the incident light....and why...and the same for low intensity too.

That's why it would be important to know the sources.

Yes but....can you please tell which one is true then?


text:
Is there any evidence that mammalian ears can act as thermal receptors?
Some snakes have a "pit organ" capable of sensing infrared radiation. The structure is similar to a primitive pit eye. Snakes are cold-blooded and their prey is generally warm-blooded, so it is obviously a useful organ to possess. The need for mammals to possess such an organ is not so obvious.
Many mammals such as rabbits, deer, bats, etc. have large ears with a parabolic form, presumably designed to reflect short wavelengths (high frequencies) into the ear canal. The inner surface is usually smooth with some protection provided by sparse hairs.
I understand that large external ears can be involved in thermoregulation, but that is not the question.
The parabolic form can also be quite useful reflecting and concentrating infrared radiation. To be effective, the external ear would have to have a smooth inner surface and to stay relatively cool. The heat-sensing nerves, if they exist, would have to be concentrated near the enterance to the ear canal. Again it would be helpful if these nerves could be kept relatively cool, perhaps on a projecting fold of flesh.
Mammals are relatively warm which already makes thermal sensing much more difficult.  Humans can easily sense the difference between facing a warm pavement versus a cold sky, though I doubt that our ears play much of a role. But could, for example, a rabbit, in the pitch dark, sense the stealthy approach of a predator or sense the entrance to its own warm burrow, just based on the thermal signature picked up by its ears?
[edit] There is a structure called a tragus in bat ears. It is described as playing an important role in echolocation, but it's also in the right position to be a thermal sensor.
Flying insects will be warm compared to their surroundings and the bats external ear may be quite cool.
[edit 2] Vampire bats have thermal sensors that are used to locate hot areas (blood close to surface) on their prey. But these seem to be concetrated in the nose-leaf and not particularly near the ear orifice.

It doesn't seem likely given the distances over which the distances surface mammalian prey and their predators operate. The most likely candidate would seem to be mice given the common environment that they operate in with snakes equipped with such senses. However, mice have no need for it since as prey, mice neither hunt nor could they use such a sense as a defense against snakes.

@DKNguyen Agreed. It's difficult to identify exactly what might drive the evolution of such a capability in mammals.  But even a mouse might find it's useful to sense its thermal surroundings in the dark while not making any noise. It would be easy to check to see if there are thermal receptor neurons clustered close to the opening of the ear canal.

Unfortunately usefulness doesn't seem to be sufficient criteria for evolution. Many things are useful. It would be useful if mice could also fly or breathe underwater, for example. But evolution seems to prioritize necessary and even already present but not too much of a hinderance over useful.


text:
Good source for current taxonomic keys
I’ve recently taken back up my interest in entomology and taxonomy. I used to be a biologist, but have long since moved to another field to make my way. I realize that all of my taxonomic keys are likely way out of date as they are mainly from the 1970s and earlier. So I’m looking for keys mainly dealing with the order Neuroptera in insects. Does anyone know where you can obtain current info?

There's the International Committee on Zoological Nomenclature, which has ZooBank, a collection of publications on nomenclature etc.  Keys would strongly depend on where you are in the world. Have you checked out the external links on Wikipedia for Neuroptera? Looks like some candidates there.

Thanks bob1, those two leads are what I needed.


text:
What is the evidence that women experience a larger cortisol spike than men, when they see domestic clutter?
I'm reading a book "The Organized Mind: Thinking Straight in the Age of Information Overload" by Daniel Levitin.
At the beginning of chapter "Organizing our homes" he says that compared to men, women experience larger cortisol spike when they see mess. I googled that statement, and the source of that claim seems to come from https://doi.org/10.1177/0146167209352864
I don't have the access to the journal, but the abstract doesn't say much about how cluttered is the home. It just seems to correlate linguistic patterns with cortisol level.
But someone stressed for sure has different way of speaking than someone chill. No clutter scale is mentioned. The person might be stressed by something unaccounted in the research.
So please, can someone with journal access and proper qualifications tell me:

Was my googling attempt succesfull, or are there better sources?
If this is the most relevant paper... is it of quality? Or my remarks on it are valid?

The full test may be requested from the authors via ResearchGate.

To be fair, this question may be a better fit on [psychology.se]. You'd need to show your prior research there (as you should here too).

I don't pretend to understand the article, but I do have access. They compared usage  of "stressful" and "non-stressful" words used to describe their houses compared to words used to describe their gardens - the words were grouped into "clutter" "unfinished" and "restful"

I’m voting to close this question because, despite the title, this is a question about the contents of particular publication rather than one about biology.

There is a freely available version of the paper available here.

I linked to the paper above in a comment.
I'm not a behavioral scientist. So interpret with a grain of salt.
The study analyzes language used after tours of homes, to evaluate how stressful the homes appear to be. So it's an imperfect measurement probably, but in direct reference to their homes. It probably does reflect something about how stressful they feel their homes to be, but IDK.
Assuming that the slope of the diurnal cortisol curve is a meaningful measure (seems to be somewhat true based on my non-exhaustive search), and that the sample is adequately powered (n=30 couples, which is not too awful but not great either given the number of hypothesis tests). If you look at Tables 1 and 2, it does look like women are affected by a "stressful home" to a degree that men are not. Men also seem vaguely unhappy about stressful homes, though not as strongly as women. Granted, they only present regression tables, which is not always very helpful for understanding causal or statistical relationships.
Nonetheless, the paper seems well-cited in the literature (as might be expected if it made it into a book). A lot of the work citing it is saying things along the lines of "we need more work in this area to examine this effect". A small number of studies seem to confirm qualitatively that messy homes are stressful for women, see for example here or here. It is less clear that the same isn't true for men, but then the majority of housework and caregiving responsibility is concentrated on women.
Furthermore, it does seem like global cortisol differences in men and women are not surprising, and that cortisol-induced stress may affect women and men differently.
Generally, this study seems ok if not great. It fits into a broadly supportive narrative of (partially qualitative) research. The sum of the literature that I've skimmed very briefly cites this paper with approval, if perhaps making more of the results than is merited given the level of power for the study. No one has posted on pubpeer about it or found anything dodgy about the study, in spite of its relatively high profile, so it's not obviously awful. I don't love the linguistic analysis either, but clutter is itself subjective I guess.
There remains the issue that you raise that perhaps a person under stress will react more strongly than someone who is more relaxed. But it's a bit circular of course- in either case, it seems like women are more stressed, and they also get more stressed out about domestic clutter.
Interested to hear more from a real behavioral science professional. I hope that my answer doesn't discourage anyone with more credentials from posting.


text:
Does aerobic exercise increase the incidence of disease via free radicals?
Aerobic respiration produces ROS, atleast one of which (the hydroxyl radical) cannot be neutralized by any known antioxidant and is always damaging surrounding tissue. I know ROS plays a role in signaling, positive feedback loop for growth/adaptation to increasing mechanical stress.
Increasing aerobic respiration through aerobic exercise (i.e. running) produces more and more ROS. Wouldn't this then increase subcellular damage and increase the risk of disease, as compared to somebody who is sedentary?


text:
Are all unicellular eukaryotic organisms protists?
I know that the Protists are in Domain Eukarya, and that some protists are unicellular. Are there any other eukaryotic group of creatures that are not protists that are unicellular?

Two other kingdoms contain unicellular organisms.
Some fungi, such as yeasts are unicellular.
Many algal (Plantae) species are unicellular, including the spectacular Valonia ventricosa, which is up to 5 cm (2 inches) in diameter. There is also a genus of seaweed Caulerpa, which is unicellular, though multi-nucleate that is thought to be the largest single-celled organism, being up to about 3 m (10 feet) long.

Not the kingdom decides, hence


text:
Are there any plants that retrieve energy from the wind?
Many trees grow in windy places, but appear to have adapted to this by developing characteristics that provide resistance to wind.
Are there any plants that appear to have been selected for the ability to obtain appreciable amounts of energy from wind, apart from propagation of spores and seeds?

Does this answer your question? Are there known life forms that are able to transform mechanical energy into chemical energy?

Worldbuilding has a version of this question, for your interest.


text:
Can an axon recieve signal from other neuron or axon of other neuron?
As there is a very complex network of neurons in our brain so could it happen that an axon can recieves a signal from another parallel axon ?

There are indeed synapses called axo-axonic or axo-axonal that involve a synapse directly onto an axon from another axon.
There's quite a variety to these, so it's difficult to make any generalizable statements about them as a group besides the tautological fact that they involve a synapse from an axon onto an axon; like other types of synapse you'd want to first specify a brain region and source/target neuron type to start looking at their properties and likely network effects.


text:
Calculate expected heterozygocity using Wright's F statistics (here, FIS)
I try to better understand Wright's F statistics. In general, there are many derivations and many interpretations, and in books, the parameters are called differently, that's why I am struggling.
More specifically, I want to understand how the inbreeding coefficient ($F_{IS}$) can be used to calculate the expected heterozygosity $H_e$.
The following formula makes sense to me:
$H_e=2pq(1-F_{IS})$,
$F_{IS}$ is the fraction of a population where the alleles at a given locus are Identical By Descent (IBD), i.e. homozygous. For the remaining fraction ($1-F_{IS}$), the Hardy-Weinberg principle applies and the frequency of heterozygotes is $2pq$.
However, in the slides my professor gave me, the parameter $F_t$, sometimes called only $F$, is used. He called this the fixation index (which, according to other definitions, would be $F_{ST}$), but since he used it as the probability for an allele to be IBD, I assume this might be what others called inbreeding coefficient $F_{IS}$ (that is a least a common definition I found in multiple books). But in the book "A Primer of Population Genetics and Genomics", the same definition is used, i.e. $F_t=F_{ST}=$ the probability to be IBD due to remote inbreeding.
Could somebody help me with my confusion?
Anyways, in the lectures, this formula is given to calculate the expected heterozygosity:
$H_e=1-F_{t}$,
where $F_t$ might be $F_{ST}$ or $F_{IS}$, see above
Could somebody help me understand if these formulas mean the same (under different assumptions of cause) or why both formulas exist?


text:
What plants are these

These are aquatic plants. Anyone knows the name please? Well. For a week more and most of them stems rotted. So, wondering if its planted by submerged in the soil or what.

I notice you've neon tetras indicating a tropical temperature, are the plants especially meant for that or just any random plants?

i have no idea either since the seller just gave random plants different than what I ordered. I wanna know how to care for these.

Take these with a grain of salt, as it is quite difficult to tell from a single, far-away, picture, and I am no expert on aquaria or aquarium plants.
The narrow-leaved (lanceolate) one appears to be Pogostemon, possibly the species * stellatus*, though I think this should (under optimal conditions) have red stems and upper leaves. This seems to have strict requirements for growth of added CO2 and intense light.
I found a site Tropica.com (I have no affiliation with, nor is this an endorsement of, the company) that sells a lot of aquarium plants and has good listings of the conditions needed for growth, along with pictures and descriptions, so it might be worth a browse through there to see if something fits better.
The second, broad-leaved with toothed margins, plant might be Erythranthe guttata (Monkey Musk), which is a common (sometimes invasive) plant of stream margins, but I don't know how well it will grow fully submerged. It will certainly tolerate short submergings (a few days), but as an aquarium plant??


text:
Can co-mutations be potential expression quantitative trait loci (eQTLs)?
I'm wondering if it is possible to test this and how? Usually we do this for single SNPs, I wanted to know if it was plausible for pairs of SNPs. Which method would you suggest?
I want to test whether the co-occurrance of mutations has an impact on expression levels.

I'd suggest looking into tests for epistasis in eQTL analysis, here is a paper I found readily, here is another tool


text:
Introduction of critically endangered South Asian species to South America
I have in mind in particular orangutans but don't want the question to be that specific, so the answers about other species will be equally welcome.
Orangutans are endangered or critically endangered due to the rapid and dramatic loss of their natural habitat (tropical rainsforests of Sumatra and Borneo).

Have there been attempts to introduce orangutans to, say, the Amazon rainforest as a species preservation measure?
Was there any public discussion of (1)?
If the answer to (1-2) is no, is there any obvious reason for that?
No chance of taking root? Or there's a big risk of threatening the existing ecosystem once they take hold?

Highly Doubt 1 and 2. Introduction of non-native species can adversely affect local ecosystems. Might endanger or eliminate several native species.  Abingdon tortoise went extinct because of mere goats


text:
Do the foldings in the brain vary person to person?
Can the gyri and sulcus, which are the foldings of the cerebrum, vary from person to person? If that is true, then can we say different people have different types of thinking skills? I believed that the anatomy of the brains of homo sapiens were all the same (except mentally abnormal children with Progeria like syndrome) but then, why do we all have different thinking skills, as I have observed in my surroundings?
I know some depends on self created skills, but could different brain foldings be the reason?

The major structure is consistent but there is a lot of variation in the details, including the presence and absence of certain gyri:

Kennedy, D. N., Lange, N., Makris, N., Bates, J., Meyer, J., & Caviness Jr, V. S. (1998). Gyri of the human neocortex: an MRI-based analysis of volume and variance. Cerebral Cortex (New York, NY: 1991), 8(4), 372-384.

Kruggel, F. (2018). The macro-structural variability of the human neocortex. NeuroImage, 172, 620-630.

Bartley, A. J., Jones, D. W., & Weinberger, D. R. (1997). Genetic variability of human brain size and cortical gyral patterns. Brain: a journal of neurology, 120(2), 257-269.

However, it's not so straightforward to connect these to function and thinking skills; the layout of the gyri is more like a shape of a blank canvas that cortical function is then written on. For example, the location of prefrontal regions relative to gyri/sulci varies between individuals:

Rajkowska, G., & Goldman-Rakic, P. S. (1995). Cytoarchitectonic definition of prefrontal areas in the normal human cortex: II. Variability in locations of areas 9 and 46 and relationship to the Talairach Coordinate System. Cerebral cortex, 5(4), 323-337.

As does the primary auditory cortex:

Leonard, C. M., Puranik, C., Kuldau, J. M., & Lombardino, L. J. (1998). Normal variation in the frequency and location of human auditory cortex landmarks. Heschl's gyrus: where is it?. Cerebral cortex (New York, NY: 1991), 8(5), 397-406.

And I'd wager most other areas, too. So you can't map the size/presence of a given macrostructural feature to a specific function. You might instead look at cortical thickness in particular functional regions, or area associated with a particular function, rather than the "phrenology" of the folds.

Tl;DR: The folding pattern seems consistent among human species but they are not exact match when compared person to person.
Long Answer:
The folding is not random like a crumpled piece of paper. Rather it exhibits a pattern that is consistent from person to person. Research indicates that a network of nerve fibers physically pulls the pliable cortex into shape during development in utero and holds it in place throughout life. Disturbances to this network during development or later due to stroke or injury, can have consequences for brain shape and neural communication and may lead to mental disorders.
Over the past couple of years, several research teams have reported that the brains of schizophrenic patients exhibit reduced cortical folding overall relative to the brains of normal people so they are quite certain that brain shape differs between schizophrenics and healthy people. Similarly, people diagnosed with autism also exhibit abnormal cortical convolutions. Some of their sulci appear to be deeper and slightly out of place as compared with those of healthy subjects. Researchers pointed out that it arises from the miswiring of the brain.
Mental disorders and learning disabilities can also be associated with aberrations in the composition of the cortical layers. For instance, in the late 1970s neurologist Albert Galaburda of Harvard Medical School found that in dyslexia, the pyramidal neurons that form the chief communication system of the cerebral cortex are shifted from their normal position in the layers of the language and auditory areas of the frontal cortex.
The above information is paraphrased from this article but you can read the whole to get a better understanding of the topic.
Also, you can refer to below papers:

Toro R, Perron M, Pike B, Richer L, Veillette S, Pausova Z, Paus T. Brain size and folding of the human cerebral cortex. Cereb Cortex. 2008 Oct;18(10):2352-7. doi: 10.1093/cercor/bhm261
Garcia K. E., Kroenke C. D. and Bayly P. V. 2018, Mechanics of cortical folding: stress, growth and stability, Phil. Trans. R. Soc. B3732017032120170321, DOI: 10.1098/rstb.2017.0321
H. de Vareilles, D. Rivière, JF Mangin, J. Dubois,
Development of cortical folds in the human brain: An attempt to review biological hypotheses, early neuroimaging investigations and functional correlates, Developmental Cognitive Neuroscience, Volume 61, 2023, DOI:
10.1016/j.dcn.2023.101249


text:
Was there a first biological cell on earth? or a similar cell originated simultaneously around the world?
It logically follows that if life began on earth and life is cellular, then either that life began singularly or began simultaneously around the world?
What is the evidence or argument for either position?
Or is it both?

Welcome to SE Biology. On this site (for  biology researchers, academics, and students) we expect posters to conduct their own research before posting to try to answer the question themselves. You must have realized that this topic would have been raised and discussed before, and you may even find similar questions on this site. Have you looked?

@David Yes I knew this would have been thought of before however my only access to information is via the Internet and mainly Wikipedia I know there is a lot of information on the Web however it is just the Web and not an area where professional information is usually published. Not being a professional biologist I do not have access to biological papers so I thought this would be the best place where I could gather information that iam curious about. I will look through the posts on this site if you wanted to close the question.

or its a no one knows question.

The technical term for the origin of life from non-living matter is "abiogenesis". If you search this site with that term you will see a list of questions, including a very active one from ten years ago, entitled "Why did abiogenesis only happen once?". You might check this out.

@David Thanks for the referral. Having read the question that you suggested I look at. Do you think it would be possible to simulate the conditions however speculative they are, that life began with?

@David I have just looked and the question of a large scale simulated abiogenesis has been asked before.


text:
Can a person have different sex at cellular level?
I mean like every cell has a sex chromosome.So does a male with XY chromosomes has all the cells in all the organs inside his body of XY chromosomes only? And vice versa.....

Same as comment on Aurelius' answer: "sex" isn't a property of a cell. At best, it is a property of a whole organism related to its reproductive plumbing. I think that you are interested in the idea of "karyotype" and "aneuploidy", and more specifically the idea of sex chromosome mosaicism is well known.

@MaximilianPress but doesn't sex chromosome mosaicism affect the entire organism? I guess OP is asking for that but in some cells only

@Aurelius It seems like OP is talking about whether all cells always have identical sex chromosomes within an organism- OP should feel free to update if it's otherwise. Mosaicism means exactly that not all cells have identical karyotype. Mosaicism will be apparent in any collection of cells greater than 1 if any two of them differ in karyotype.

there are biological males with no Y and instead XX chromosomes. there are biological females with XY chromosomes.

Every organism(sexually reproducing) starts life from a single cell zygote formed by union of sperm and ovum.
Since all cells are formed by mitotic divisions and differentiation of the zygote, the number and type of chromosomes remain same in every cell of the body.
In rare cases however there maybe chances of aneuoploidy of the chromosomes during cleavage or later mitotic divisions. As given in the article, post-implantation mitotic aneuploidy is rare and is checked. Should it escape:

Mitotic aneuploidies have been suggested to affect the developmental potential of human preimplantation embryos, possibly leading to developmental arrest or embryo loss at later stages of development. Mitotic aneuploidies may contribute to implantation failure or when compatible with implantation, may result in fetal or confined placental mosaicism. It might also cause serious fetal complications like intrauterine growth delay, congenital malformations, mental retardation, and uniparental disomy.

If chromosomal abnormalities occur after immune system has started working, it can be taken care of.
It's rare to have mitotic aneuploidy in a  person. To have it in two chromosomes(the allosomes) is even rarer
In conclusion it will be extremely rare for a living cell to have different sex than that of the person
For plants though it is much more common.
Edit: As @BryanKrause has pointed out. Chimera are another cause. If chimera  due to organ transplant is also considered makes it not so rare as I mentioned

I don't think that "sex" is a property of a cell. At best, it is a property of a whole organism related to its reproductive plumbing. Karyotype != sex (!= gender).

Chimeras are also rare but it happens.

All women who have been given birth (or maybe past some point of a pregnancy) are effectively chimeras.  Most (if not all, haven't bothered to search for exceptions) such mothers have cells containing the DNA of their children in their bodies for years (if not forever) after the birth.


text:
Plant (lamp) identification
I recently came across this lamp part and wanted to get a lamp shade in the shape of the matching blossom.
Does someone recognize the leaves?

Flower bracts are wrong, but Thistle springs to mind. May not represent a real plant after all.

It looks to be a poppy, possibly the breadseed poppy
The flower has 4 perianth segments remaining after anthesis,matching the breadseed poppy where the sepals are abscised during anthesis leaving 4 petals.
the leaves are toothed, matching *papaver somniferum *

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. Answers on this site are typically upvoted if they contain information that supports the answer - in this case you could supply some information about the poppy, possibly including photos (proper attribution of photo source required) and why you think it is a match for the item in the photo from the question.

Different people see different flowers, interesting. Although the leaves are consistent with Poppies (good guess), the head is definitely not. At no stage does the poppy resemble that "flower". I initially thought "Tulip, but the leaves are wrong" (your guess is better than mine), bob1 thought "Thistle" (a v. good guess). The flower is either a stylized version of a flower m unfamiliar with or one that is non-existent. (I've seen a lot of flowers, as I used to travel the continent to do wildflower and garden flower photography, the latter containing plenty of non-natives)

I know, I'm a the very definition of a stickler for fine detail. Also, guesses are not acceptable in answers on scientific sites like this one. We require sources for answers.Morphology, Taxonomy, Anatomy, and Palynology of the Opium Poppy (Papaver somniferum L.) Cultivation in Northern Thailand.  Note figs. 3 and 4

It may be a general rendition of a poppy rather than a specific poppy.                                               Tulips have perianths with six tepals and thistles have capitulums

Poppies have 2 sepals  (which fall off before the flower opens) and 4-6 petals, and they don't look like those. We can't identify it; it probably doesn't exist. The good news is you can make a lampshade however you want! :)

The 4 petals of a poppy match quite well with the lampshade

I will admit to being wrong if somebody shows me a better match

Why don't you post a photograph of a poppy blossom (any poppy blossom, not necessarily breadseed poppy) with pointed petals? That would help with your answer's credibility.

What do you mean by pointed petal


text:
Why doesn't treating neurons with a high sodium solution depolarize their membranes?
I am reading a journal paper, and in one of their experiments they treated organotypic hippocampal slice cultures with a high potassium solution to depolarize the neuronal membranes:

We found that the medium from control slices, transduced with
AAV-CMV-LacZ, incubated in high potassium solution (+20 mM) over 24
hours contained statistically significantly higher IGF1 than that in
high sodium solution (+20 mM), consistent with our hypothesis that
IGF1 is released from pyramidal neurons in an activity-dependent
manner.

I know that increasing extracellular KCl concentrations is commonly used to depolarize neurons in experiments. I have read that the resting neuronal membrane is highly permeable to K+, and that the membrane potential is sensitive to changes in extracellular K+ concentration. Increasing extracellular K+ depolarizes membranes.
This is due to the influx of K+ ions through potassium leak channels (though neurons also have voltage-gated K+ channels, I'm assuming that they have more potassium leak channels).
Under resting conditions, there is a higher concentration of Na+ ions in the extracellular fluid compared to the cytosol of the neuron.
At rest, both the electrical and diffusion forces are driving Na+ towards the inside of the neuron (since the inside of the neuron is more negatively charged compared to the extracellular space).
In the paper, they incubated neurons for 24 hours in serum-free medium plus 20 mM NaCl.
However, increasing extracellular Na+ levels did not depolarize the neuronal membrane (unlike increasing extracellular K+ levels).
Why is this the case? I know that the neuronal membrane contains voltage-gated sodium channels and sodium leak channels. Is it because neurons have a higher number of voltage-gated sodium channels in their membranes compared to sodium leak channels?
I.e. to depolarize the membrane, the Na+ leak channels are not enough, you also need the opening of the voltage-gated Na+ channels.
Any advice is appreciated.

I would start with the Goldman equation, plug in some reasonable values and experiment with the results. Your reasoning I think comes from a common misconception that involves counting positive charges and forgetting that any solution with sodium or potassium cations comes with an equal balanced number of anions. You're never adding just sodium or potassium; if you did, you'd have enough energy in a small solution to create lightning and the charges would rebalance themselves. Membrane potentials are based on really tiny charge imbalances.
Potassium is high inside cells and low outside; if a cell is only permeable to potassium, that would mean a bit of potassium leaks out, following that concentration gradient. The result is a cell that's a bit negatively charged inside. If you increase the potassium concentration outside to equal the inside, there's no concentration gradient for those ions to travel down, so no membrane potential. If the potassium concentration outside is greater than inside, potassium ions flowing down their concentration gradient results in a positive charge inside the cell.
If there is little sodium conductance, changes in sodium don't affect the membrane potential. If you add a bunch more sodium outside, it will depolarize the cell a little bit if there's some sodium conductance, but as long as most of the conductance is for potassium it's mainly the potassium concentration gradient that matters.
Also, this experiment is just adding 20 mM additional sodium or potassium extracellularly; for potassium that may be doubling the concentration or more. For sodium it's more likely a 10-20% increase.


text:
What kind of insect appears in this photo?
For months my wife has been commenting about a white substance spontaneously appearing on black clothes. Under magnification, the substance appears to possibly be eggs. As you can see, the image shows a structure smaller than 0,1mm on her jeans fabric.

My clothes are unaffected. We live in Neugraben, a south-west suburb of Hamburg. We do not have any pets.

You'd be surprised how often it happens that people forget to post an image of what they're referring to.  When you add yours, could you also fill us in with a few details about where in the world are you - which country and if you're in the city, the suburbs, the countryside for visits. Do you have any pets or pests around the house/loft/walls?

Friendly note on English time expressions of this type, which are one of the top three traps for non-native speakers in my experience (in an international science laboratory). "Seit zwei Monate", "depuis deux moins", "da due mese" translate into English with the pronoun "for" — never "since". (And generally with a past tense, here a past continuous "has been complaining".)

#1: I am living in Neugraben, a south-west suburb of Hamburg. We do not have any pets.

looks like a ball of lint to me.

I think these could be the eggs of woolly aphids(Eriosma lanigerum), which overwinter and spend their winter as either nymph or egg , woolly aphids usually lay their eggs in autumn .They are mostly attached to the stem of young plants and some species on Apple trees also and their size is about 0.3mm to 0.6mm (of eggs).
These are not harmful or poisonous to humans and not so for trees but species are like Eriosma americanum "Eriosoma lanigerum - Wikipedia" https://en.m.wikipedia.org/wiki/Eriosoma_lanigerum


text:
Why is coconut a fleshy fruit?
Firstly, I understand that it is classified as a drupe and its mesocarp is fibrous hence its hardness. However, how did botanists conclude such? Putting both mango and coconut side by side, we can at least see that the mango has fleshy mesocarp and soft exocarp. I would argue that the coconut's structure bears more similarity to the durian yet the latter is a capsule (or dry).
With that in mind, I cannot comprehend how the pericarp is distinguishable in 3 layers in coconut but not in durian yet they seem to be same? If coconut is like a deviant under drupes due to its fibrous mesocarp, (1) how'd they even distinguish that it was a mesocarp and (2) what is the clincher that made them conclude that coconut is indeed a fleshy and drupe despite seemingly deviant from common examples such as mango?
Apologies for not being articulate enough to explain.


text:
Is this woodlouse or bed bug?
I have found 3 of these things in the main bedroom within 4 days of each other. A little freaked out, can someone advise if these are woodlouse or bed bugs? and now just added another pic (first pic?) which seems to be an entirely different bug? Carpet beetle? ...that I just found in a cupboard?
I have found 3 of these things in the main bedroom within 4 days of each other. A little freaked out, can someone advise if these are woodlouse or bed bugs?

Welcome Jax. Which photo are you referring to? The reason I ask is that you seem to have 4 photos of 3 different creatures. Could you add that detail, bearing in mind we answer single focused questions one per post, and tell us whereabouts in the world you are.

Apologies, the top pic and creature was one I discovered this morning after I made my original post. I think the first pic is a carpet beetle? the 2nd pic, did wonder if that was a moth as it looks different, this was in a draw. Last two are the main ones that I was finding and my main concern as I found two on Friday and another last night. These are the ones that I am hoping are woodlouse and not bed bugs, but I am not sure?

To add, I'm in London, UK.  and sorry I didn't realise you are meant to have single focus questions. To be honest I thought pics 2-4 might be all the same, but your suggestion 3 different types made me question the one from the draw which I think could be a moth.

The insect on the first image is a ladybeetle, likely the Asian ladybeetle (Harmonia axyridis), a species which is well-known to enter buildings, especially for overwintering.
The subsequent photos likely depict the larvae of a carpet beetle - compare to this answer here.

You say the subsequent pics show larvae beetle, but when I look at that link, it looks like the one from the first pic?  Can someone clarify what the bottom two pics are? i.e one on the wall and one of the grey fabric

@JaxConrad The bottom two are very likely carpet beetle larvae. Google "carpet beetle larvae" (without quotes) and click on the tag underneath, images.


text:
Insect Identification Request -- brown and white flea-like bug
So for context, this is a bug I found on the leaf of one of my young ginger plants, which I found a few days after watering. I have a few other tropical plants next to it, like a vanilla bean orchid -- which has the original soil from the garden store, unlike the ginger. (No bugs on the orchid btw).
The bug I found is a small (around the size of a pencil tip) jumping beetle. When I put it on a piece of tape to take a picture, it bends the end of its abdomen over its back so much that it is almost folding.It is also the only one on the plant that I found.
Some photos below (sorry about the poor quality):

hard to say from the photos; could you do ones which aren't washed out?

Where are they from?

@bob1 What do you mean by "washed out"? Do you mean the brightness/contrast of the photo? If so, I don't have any like that, because unfortunately this was the best I could do with my crappy phone camera.

@bathyscapher I'm not sure where the plants are from, but I live in central Canada.

Great, thank you. The location is usually more important than the origin of the plants (but latter sometimes might help as well) :)

These are clearly the larvae of the suborder Auchenorrhyncha, to whom cicadas, leafhoppers, treehoppers, planthoppers, and spittlebugs belong:

the have an (usually) elongated body shape, often with a triangularish abdomen which is often bent up at the tail
they have a well-developed, sclerotized pronotum
they have characteristic piercing-sucking mouthparts located on the front of the head used for feeding on plant sap
they usually have relatively short antennae
their eyes are well-developed and positioned laterally on the head
their legs are adapted for jumping, with hind legs being particularly muscular
as hemimetabolous insects, their larvae lack wings and their segemented bodies are visible all around their abdomen

These characteristics can be seen here in this (german) labeled image of an adult Neophilaenus lineatus (image credits:  Elke Freese | CC-BY-SA-2.5,2.0,1.0:

All these characteristics match well, therefore I conclude they must at least be Auchenorrhyncha. But even more, it is possible to identify them as leafhoppers (Cicadellidae):

both adults and larvae, have a slender and elongated body shape
usually, they are small insects (few mm to around 1.5 cm)
they have each pair of compound eyes and of dot eyes (ocelli) on the top or front of the head
the thickened part of the antennae is very short and ends with a bristle (the so-called arista)
the femora are at front with, at most, weak spines.
the (mostly squarish) hind tibiae have one or more distinct keels, with a row of movable spines on each (so-called setae)
the tarsi have three segments
the front wings not particularly thickened.

Here is a close-up of a leafhopper larvae (image credits: Patrick_K59 | CC-BY-2.0) depicting most of the named characteristics:

Thanks for the help! Just to add something too, it looks like leafhoppers (especially the larvae) curl the end of their abdomen like what I was seeing

Indeed, some species do curl their abdomen.

I think this is a springtail which lays it's eggs in young plant and moist soil and as you said, It bended it's abdomen by placing it on tape ,when they are stimulated ,they open their hidden tail known as furcula to save themselves from predator. I hope it is

Thanks, I think that is right. I searched a bit for some coloured springtails, and I found one that looks somewhat close, at least in terms of legs and hair (and that it is a springtail with a pattern; I haven't heard of that before):  Entomobrya nivalis (https://tinyurl.com/4xs3rsse)

Also, is the furcula the thing that looks like another leg, but singular, in the right side of the insect's body, on the first picture?


text:
How frequently does recombination occur, and how long are the recombinated fragments?
I understand the mechanics of recombination, but am struggling with the 'scale'.

When two homologous chromosomes pair, roughly how many recombination events occur on average? I understand there will be a distribution, and it will vary between species - but are we talking one, two, or hundreds/thousands?

How are long are recombination fragments relative to the entire length of the chromosome? With the same caveat as above, I'm trying to get a sense of scale - 0.001%, 1%, 10%, 25%?

When crossover happens, it's a whole swap from that point on, not just a little chunk. So if there's only one crossover event, then the lengths are "p" and "100% - p", where p is the position along the chromosome. The only way to get a small piece of one chromosome amidst a mostly intact copy of the other would be for there to be two crossovers close to each other.
This existing Q&A talks about the rate of crossovers in human chromosomes:
How many recombination events are there per generation in humans?
It varies by which chromosome you're talking about and other factors, but something along the order of 1 to 4 events per chromosome would be a reasonable ballpark. 0 is possible, too.


text:
Is repeated exposure to near/mid/far infrared safe for skin and eyes?
I've been doing a lot of research into infrared saunas as they've risen in popularity. I've come across a fair amount of information about how harmful near infrared exposure can be to the eyes.
This study was done on rabbits, and doesn't differentiate between near/mid/far, but concludes that, "The protein of eye lens is very sensitive to IR radiation which is hazardous and may lead to cataract".
This research published by Berkeley does differentiate between near/mid/far and indicates that near poses the greatest risk to the eye.

"Near‐Infrared Exposure and Cataracts The most common eye disease
associated with near-infrared radiation is cataracts. Prolonged
exposure to IR radiation causes a gradual but irreversible opacity of
the lens. Other forms of damage to the eye from IR exposure include
scotoma, which is a loss of vision due to the damage to the retina.
Even low-level IR absorption can cause symptoms such as redness of the
eye, swelling, or hemorrhaging.
Cataracts caused by near‐infrared radiation have been noted
historically in glassblowers and furnace workers. Radiation between
800 and 1,200 nm is most likely responsible for temperature increases
in the lens itself because of its spectral‐absorption characteristics.
Visible wavelengths may also contribute to the problem, since the heat
absorbed by the iris could result in heat transfer to the lens.
Acute Skin, Cornea, and Iris Injury IR radiation below 3,000 nm will
penetrate into different depths of the cornea to varying degrees,
depending on the specific wavelength. The iris can absorb energy only
at wavelengths below approximately 1,300 nm.
IR thermal injury may have significant biological effects on the human
skin. The IR-A rays induce free radicals in the dermis and diminish
the skin’s antioxidant capacity, the main cause of premature skin
aging.
Both the skin and the cornea are opaque to wavelengths >1,400 nm.
Exposure to IR radiation in this region causes injury through thermal
mechanisms, with absorbed radiation being converted to heat."

But, it's hard to understand if this would translate to consistent usage of saunas that leverage near/mid/far infrared. In the case of the Berkeley research, it's looking mostly at workplace hazards (welding, etc.), which in many cases would require participants to have their eyes open and very close to the heat source. But if the issue is simply that infrared heat is penetrating and heating the cornea, it would seem that that could be an issue for saunas as well. It also seems to indicate that even far infrared would be damaging to the skin, when sauna companies are claiming the exact opposite to be true.
I find it quite alarming that sauna companies are touting near infrared as a "plus" when it sounds like most research points to it being harmful in the long run.
My question is this: does anyone know if far infrared is conclusively safe for the eyes and skin in repeated use in something like a sauna? Is near infrared really the risk? Or is how saunas are using it below some threshold of safety?

It would depend strongly on the intensity of the source. The cataracts for furnace/glassblowers are from high intensity sources in relatively close proximity - close enough to get splashed with liquid metal according to the historical documents.

https://en.m.wikipedia.org/wiki/The_dose_makes_the_poison

Forgot to add, our eyes are always exposed to IR while we are alive - our bodies are warm after all, and IR is the "heat" wavelengths of radiation. There is also ambient heat wherever we are.


text:
Why can't fish extract oxygen from air?
I've read many posts here and elsewhere for example:

Wikipedia where breathing is well described, but does not answer the question (or anything close.)#
Wikipedia Gills, more specific, but still doesn't answer the question
This blog post
Several Quora's blogposts including this one.
Also some Youtube videos like this one

and I do not think that the fact that gills surface / contact area is larger with water wrt to air fully explains the reason why they can not breathe in air.
I wonder if one possibility is that they do not control the bones that open the gills (I don't know the name.) since they seem to use the water pressure to some extent for that matter.
Is there a more detailed explanation that you can offer, or point to?

What about how fish gills collapse in air? And they have no way to pass air over their gills? Or how gills dry out?

@DKNguyen gills have still a lot of surface area, and more oxygen density; for the dry out, that's a second question, but not the main one.

Surface area doesn't mean much if your gills collapse.

Drying out is not a separate question.

The microstructure, too small to see with the human eye absolutely collapses to a small fraction of its surface area. Just to note: 1) Prior research is a requirement when posting, 2) the purpose of comments isn't to be "interesting", or to make derogatory remarks, it is to request clarification from the OP and to provide direction to new contributors those who may lack familiarity with the site's ways and with the topic.

What you've cited is blog-posts and Quora threads, not scientific papers or from scientific journals. I've requested that you show your prior research, please do so - bearing in mind that we accept scientifically credible sources (Wikipedia is a secondary source but a good place to start as they have references you can follow-up on). I've also explained to you what comments are for, they are not for answering the question (with or without references).

They are not considered credible on this site or any scientific site on the network.

There really isn't any discussion to be had, I'm just trying to help you to use the site the way it's intended. You can read the [ask] section of the [help] for clarification, or wait for "someone more knowledgeable" if you wish.

The blog-post is fine, seems credible to me, as far as it goes, but it's very broad and not specific to your question.

added 2 relevant sources that i read completely and you asked for @JiminyCricket.

From the Wikipedia page on gills that you link:

The density of the water prevents the gills from collapsing and lying on top of each other, which is what happens when a fish is taken out of water

Wikipedia's source for this statement is a biology textbook: M. b. v. Roberts; Michael Reiss; Grace Monger (2000). Advanced Biology. London, UK: Nelson. pp. 164–165 though I'm not able to access this source.
You need a lot of surface area for gas exchange. If the gills collapse as they do if not submerged in water, there's not enough surface area for gas exchange. If you did somehow spread them out mechanically, they'd dry out. You might think about how a net can sit expanded in water, but if you pick it up it all bunches up; same as gills.
Other sources:

Gills are very delicate, almost paper-like structures that depend on the buoyancy of water to remain open. The fragile gills will collapse if the fish is taken out of the water because air doesn’t have the same density and buoyancy water has to keep the gills open and functioning. This is why a fish cannot live outside the water.

https://blog.limnology.wisc.edu/2016/09/14/at-home-in-the-water-condemned-to-life-on-land "This essay originally appeared in the Lakeland Times in Minocqua, Wisconsin. Carol is an Aquatic Invasive Species expert and outreach specialist with the CFL and Wisconsin DNR."

A paper on a fish with modified gills that allow it to breathe in air:

The bowfin, Amia calva is a facultative air breathing fish restricted to North America and is reported to estivate. ... The secondary lamellae are fused to form a lattice-work of rectangular pores, a gill arrangement unique among freshwater fishes. This highly modified gill structure imparts considerable rigidity such that these do not collapse upon air exposure.

Daxboeck, C., Barnard, D. K., & Randall, D. J. (1981). Functional morphology of the gills of the bowfin, Amia calva L., with special reference to their significance during air exposure. Respiration Physiology, 43(3), 349-364.

What is being said here, is not how one should reason imho it's at best suggesting that they correlate. Yes, they collapse and the surface area decreases, we all know that, it's even included in the post, so doesn't add anything new. Maybe the source has some extra details. Currently, this isn't at all an answer. Feel free to downvote again, since that's how people reason here apparently.

I will also add, that I do not find that quote, or even an equivalent statement, in the linked article from Wikipedia (not a book as you said, and we should include the source if it is open source): https://evodevojournal.biomedcentral.com/articles/10.1186/2041-9139-3-24

@MahNeh The source is the one that I posted in my answer (ref "#4" on the Wikipedia page), which is a book, not the link you have ("#7") - not sure why you're looking at that one. And no, this is not saying that they merely correlate. Surface area is critical for gas exchange and causal for sufficient gas exchange. Surface area of gills decreases massively in air, to the point of insufficient gas exchange. That's the answer. If you want a different one, that's not likely to work out well.

In any case, you should have include the source of your claim. And for the blog-post you include that's a simple paragraph, not an experiment. I don't just follow possibilities as if they were true. If that's a theory, must be validated, the link you should is not the validation, so it's wrong and not an answer.

@MahNeh I did include the source: Wikipedia, as well as Wikipedia's source. I've now included a couple other corroborating sources. The idea that surface area is important for gas exchange is quite trivial physics, but isn't something you asked about. I'm not sure what experiment you're looking for, this is something that anyone looking at gills can observe: they collapse in air. We know that surface area is critical for gas exchange, so observing the collapse is all you need to do as an 'experiment'.

I am a physicist, and don't need explanation on that (as I said, it was included in the post since the beginning.), because that's not the only variable here, but I don't think this is any good, and won't bother helping more. Bye.

I hadn't downvoted your question before but now I will as I see it has not been asked in good faith. Good luck.

@MahNeh - Please define ignorance, because the user answered your question definitively, with sources. That's generous and informative, not ignorant, unless your definition of ignorance is different from mine. You have repaid the user with insults.

Please, re-read the comments @anongoodnurse

@MahNeh Do you buy the reasoning that human lungs work in air but not underwater because they have do not have enough surface area for lower oxygen levels in the water, but have measures to prevent collapsing when not submerged? I am not sure any answer will be good enough for you since it sounds like you want comparative artificial or mathematical models of what are biological structures and technology just has not enabled those to be as readily available in biology as they are in physics.

@MahNeh Should she re-read the comments where you're confused between reference 4 and reference 7, and what should she conclude from those?

@DKNguyen, sorry I am tired. Thanks though, geniuses, for explaining to a simple man.

@BryanKrause she should read tribe behaviour, then you will understand how you behave, as the monkey with the stick. Take care.

Fish can't exchange gas efficiently in air with their gills.  However, many more fish can breath air than people often think, even those you wouldn't normally think of as "air breathing", but they don't use their gills.  All bony fish have a swim bladder, a sort of internal water wing that fills with air and allows them to remain suspended in the water column at rest.  Fish can change their buoyancy by diffusing gasses into or out of the blood, changing how full the swim bladder is.  So, you actually have something that does almost all the stuff lungs do.  It holds gasses and allows for them to be exchanged between itself and the blood stream.  Give it a way to be filled from the outside and you have a simple air breathing system, and many fish do just that.  They gulp air and have some way of getting that gulped air into their blood, either from the stomach or the swim bladder.  A lot of fish who live in murky water or water likely to be somewhat de-oxygenated not only are able to do this, but need to.  Beta fish will actually drown if they are blocked from surfacing to gulp air.  So yeah, lots of fish, even ones that you don't think of as "air breathing" can breath air, but they don't tend to do so with their gills.  Some gas exchange can still happen through the gills so long as they remain moist, but you need something that won't collapse or dry out to actually be able to breath out of the water.


text:
How to pit viper pits maintain high sensitivity across a wide temperature range?
Pit viper infrared vision works nothing like our photochemical rods and cones. It would be blinded by its own thermal noise it if did. Instead, they are sensitive to changes of temperature [of only 3mk][1] across a wide range of body temperatures (17C to 37C for the poikilotherm snakes).
How do the cells detect tiny changes in temperature but be insensitive to slower but 1000-fold larger temperature changes?
[1]: https://journals.physiology.org/doi/full/10.1152/ajpcell.00040.2004#:~:text=Multiple%2D%20and%20single%2Dunit%20neuronal,15%E2%80%9337%C2%B0C).


text:
Identifying a bone I found in Central France
I found this bone in Auvergne as a child. This specific area is apparently well-known to paleontologists and I found the bone in a field very close to scientific excavations (literally meters away from the area that was delimited by ropes). I picked it up and brought it to a local museum but back then they simply told me something like "lucky find, it might be a prehistoric animal! You can keep it, we only do mammoths here."
Years passed and I've kept this bone (probably a vertebra, coccyx or sacrum) on a shelf. Now, my curiosity is having the best of me and I would really like to identify it.
I spent some time looking at "bone identification" forums, databases and charts online, but they were quite disappointing. However, I am almost sure the bone belongs to the spine of a mammal.
Here are pictures (mug for scale):

Definitely spine, pretty certain on sacrum too, which most likely makes it mammalian (given location...), but have no idea on species. Might not be identifiable as lots of it is missing.


text:
Strange Mitotic phase of oocytes in primary follicles
In the process of learning about the reproductive system, I find  an oocyte enveloped by a single layer of follicular cells appears to be undergoing equal division, resembling a primary follicle located near the ovarian tunica albuginea. This slice is from rabbit ovaries, stained with HE, 40 * 10.
What puzzing me is: It seems that the oocyte should not undergo mitosis at this time, and I am not sure how to explain this phenomenon?
My initial idea is whether it is possible to have multiple oocytes simultaneously in the follicles of rabbits. I tried to searche on PubMed and Google, but found no relevant evidence.

PS: Because the file size is limited to less than 2M, the image here only captures a portion of the field of view. If you need a complete picture, please leave a message.


text:
What species are these, beetle eggs?
I posted a thread the other day and identified I have carpet beetles larvae. I have a pest control company booked to treat the place on Monday but in the meantime I’ve found these little things on the wall that keep appears and I’m wondering if these are the eggs stage of the beetles or perhaps an entirety different species? Someone on a Facebook group suggest they could just be wax or food, but how would either randomly just appear on the walls?
Size wise they are about half the size of a grain of rice or perhaps a little bigger.
Just been googling, could it be instar stage of bed bugs?
I’m based in London, UK.
enter image description here

enter image description here

food (or snot-stuff) can appear to 'randomly' appear (i.e. appear unexpectantly) on walls or ceiling simply from a cough or a sneeze

These are not instars or eggs. These are debris from food or perhaps ear wax or something similar.
If they were instars you would see either a uniform larval shape - usually bilaterally symmetrical, or you would see something that indicated a body form like legs, head etc. You would also expect that they would be about the same size and shape in each case, though different age/stage larvae can have different sizes.
If they were eggs, you would generally expect them to be both the same size and both the same shape if they came from the same species. They would also be very large eggs for common insects; most butterfly eggs for example are in the 1-2 mm range, rather than 5-7 mm.


text:
How could an aquatic animal’s organ evolve so it could live outside water?
How could a fish’s organs evolve so that it could one day live outside of water.
I mean did it one day fully evolve then stick its head out of the water. That would mean that all the evolution of that fish would have needed to happen while it was essentially under water. But I can't see how that it is possible to convert from aquatic to semi-aquatic while living in the water.
Surely its organs would fail while only living in the water but having dual-function lungs and other organs.

Welcome to Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. In particular, note the homework rule - So, what do you know about evolution of the lung? As a hint, you might want to investigate respiratory systems in fish, particularly Lungfish.

look at fish that live in swamps they breath air because the water is so low in oxygen. we think lungs and legs both evolved in the water.

Which organs? the skin is watertight in most fish to prevent dehydration to saltwater. the only organs exposed to air are the eyes, skin, and whatever they breath with. if you look at US one of those is watertight and the other two constantly lose water.

It may surprise you to learn that most bony fish are capable of breathing air, not just the lungfish and mudskipper.  If you have ever seen a fish in a muddy lake looking like it's blowing bubbles on the surface, that is what was happening.  It was breathing.  Oxygen levels in the water can be super inconsistent, and many fish species need to be able to supplement that oxygen with oxygen from the air in order to survive.  If you ever get a betta, make sure it can make it to the surface because it will straight up drown if you don't.  The way they tend to do this is via the swim bladder.  The swim bladder is already almost a simple lung.  It can hold gas and exchange it with the blood.  All you need to make it a basic lung is a tube that connects it to the mouth.  Throw in some branches and ridges for surface area and you have a full on lung right there.  Some fish can fill the air bladder directly by gulping air.  Others gulp it into the stomach and then diffuse it into the air bladder, but most fish can breath air to some degree, even if they never come out of the water.  Fish that do come out of the water, like lungfish, do so using a modified swim bladder, one with a tube and some nifty ridges that lets it function as a full lung so the fish can go for a walk when its pool dries up.  From there, it's just more ridges, more pockets, more surface area, better tubes, basic optimization that evolution is real good at.  The line from swim bladder to lung is actually one of the straighter ones when it comes to evolutionary history.  There are definitely some winding roads but this isn't one of them.


text:
If split peas are good for health, why didn't evolution favour humans liking split peas?
Split peas, being legumes, are a source of food unanimously considered as healthy. My question is why didn't evolution favour humans that liked the taste of split peas? And/or maybe that could eat split peas raw without cooking them? Those humans would be favoured since they wouldn't have to cook them and/or would be favoured because they would eat plenty of this healthy food since they like it?
Forgive me if that's already been answered but sometimes I have those questions which I don't find answers to and it puzzles me.
EDIT: I'm not saying that split peas taste bad, but for most people, it does not taste as good as nuts, which are healthy too, for example (no source but I think most would agree)

Remember the prior-research requirement, see lectins.

Don't mistake evolutionary solutions for optimal ones. You need selective pressures, pre-existing mechanisms to work with, and luck.

I love split peas. I love lima beans more, and would happily eat brussel sprouts every day. I don't like apples. I like a few kinds of nuts but nowhere near as much as brussel sprouts. Yet I am an end product of evolution. Did I "devolve"? Or is your opinion only that: someone's opinion?

In the ~500 million year evolutionary history of taste buds, or even in the ~2 million year evolutionary history of humans, how long have we been eating domesticated peas? Maybe like 10,000 years. And by that point we were probably manipulating their evolution through agriculture. So the question should be, why didn't we select for peas to taste better?

@MikeyC or the question could be, Why did split peas/legumes evolve to taste bad? or perhaps Why are most legumes not edible raw? There I can see selection pressures..

Because our modern nutritional needs are different than the ones we evolved with. Also cooking.
For a lot of our evolution, food was a limiting factor. Our ancestors regularly died of starvation, and sustaining sufficient calorie input was really difficult.
Part of the evolutionary "fix" for this is a preference for calorie dense foods - like nuts, or sweet tasting things, or, say, fatty cuts of meat (mmm, bacon). This is reflected in types of taste receptors (sweet, protein rich, and salty all trigger different receptors), and our brain wiring to perceive these as good.
The second part - why do they taste bad? Well, our taste receptors are relatively crude, but have inbuilt warnings - bitter is often "this food is off" but can also be "there are toxins in this" - Our receptors are relatively indiscriminate in the flavours they pick up on.
The third part is that humans, fundamentally, are weird. We like powerful chemical irritants (chilies, peppercorns), signals of decaying food (cheese, alcohol), and a whole range of other things that animals with less curiosity would have treated as the dangerous substances they deserve to be. So our tastes are built up from some hard wired stuff (mmm, sugar) and some social or learned stuff (mmm, moldy, solidifed cow's milk)
When we also throw cooking into the mix, humans eat a wide range of things our bodies are not well adapted to eat. But, the wiring for taste receptors remains pretty similar to before cooking, so they throw up false warnings - this bean is indigestible, and contains a bunch of bitter things that might be poison. This round, bitter bit of brassica has few calories, but a bunch of minor toxins, so we reject it. Eating enough of them raw will upset our stomachs, at the very least.
But, we can learn to like things - and some of that is us forming good associations with the food we're eating, and some of it is a dampening down of the warning signals - eat something bitter regularly, and your brain stops going "shit, you're trying to poison us" and instead starts realising it doesn't get sick from this particular food

There are a fair number of questionable statements here, making this answer very much just opinion (which isn't a good fit for a science site.) If you could provide references to back up your points, it would be very helpful. Thanks.

all very fair - I think I've not got time to dig through for the sources, and it was a bit of generalization, pitched at the level the question was being asked at - think it's better to delete or leave it?