text:
Has there been a measurement of a stalling force for myosin molecular motors?
For processive molecular motors like kinesin, in vitro assays have allowed to measure directly a stalling force beyond which they do not progress anymore or detach.
As far as I know, the literature has only very indirect ways of evaluating what a stall force may be for myosin molecular motors, is this true? If so, is it because of the nonprocessivity of most myosin motors, or are there other experimental obstacles to this measurement?


text:
Calculate radius of curvature of DNA
I am using this article to calculate the radius of curvature of DNA. I know that

150bp segment of DNA length wraps itself 1.7 times around a histone core.
There are 0.34nm/bp
DNA's persistence length l is 53 nm.

How can I use this data to calculate the radius of curvature of DNA?
According to the article, $l = \frac{B}{k_BT}$ ($B$ is bending modulus, $k_B$ is Boltzmann's constant, and $T$ is temperature). However, the only way the units cancel correctly is if $l = \frac{k_BT}{B}$. Which is the correct formula?
Assuming I know $T, k_B, l$, I can calculate $B$. Since DNA is a homogeneous isotropic rod, $B$ is equivalent to Young's modulus $E$. Is there a way I can use $E$ to calculate the radius of curvature? Or am I doing this completely wrong?

According to the article E= Bl/2R^2. Does that help?

Yes, but I am then confused how to get E/I.

I'm no mathematician by any stretch of the imagination, but it seems from the paper that E~kbT, and l~B/kbT thus by substitution l~B/E and therefore E~B/l for a given temperature and if R=l. I get units for l as N.mm^-2.J^-1, but it should be just distance (nm in DNA's case) correct?

I don't think DNA has a particular radius of curvature any more than it has a particular length. It will depend on the situation. In the case of DNA wrapped around a histone, the radius will be half the diameter of the histone + half the diameter of the DNA.

source: Stack Exchange

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

sort: votes


text:
The quality of binding sites?
Can someone please provide a human friendly explanation.
to the following:

RNAp binds a defined site (a specific DNA sequence) at the promoter
(Fig- ure 2.2a). The quality of this site specifies the transcription
rate of the gene

what is the quality of the site?

Quality is most likely related to how tightly RNAp binds to conserved sequences in the promoter, and that is related to how closely the actual sequences themselves are to RNAp's "most-preferred" sequences. The actual sequences can vary between genes, giving them different transcription rates.

thank you for your explanation
much appreciated

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


text:
Pressure inside a cell
In this article, in the introduction 3 paragraph first line they said:

The flow of water plays a critical part in these processes. Recent
experiments suggest the pressure equilibrates within cells giving rise
to intercellular flows of cytosol that cells may exploit to create
lamellipodial protrusions or blebs of locomotion

Equilibration of pressure inside cell is something I don't understand. Okay, in the lamellipodium part of the cell, the cytosol were pushed to that place. It means that there is a pressure gradient so the pressure in the lamellipodium should be different in the pressure of the bulk of the cell where the nucleus is present. Some model assumes that they are equal like here.
Can any body explain what do we mean exactly by pressure equilibrates and volume conservation inside cell? Why it needs to be conserved knowing that the cell is changing its shape i.e. its area and thus the volume? Any good citations?

Seems like you'd find a lot in the papers this one cites, such as 9, 8, and 17.


text:
Non fluorescent DNA stain to visualize Drosophila polytene chromosomes
I am working on designing a lab for an undergrad genetics course which involves dissecting and visualising polytene chromosomes from Drosophila salivary glands. I need a non-fluorescent non-antibased staining for the DNA to visualize the chromosomes, as we won't have access to antibodies or an episcope (only compound microscopes). Does anyone know of a DNA dye that could work?

Giemsa stain should work. It is traditionally used in karyotyping staining. It results in G-banding.


text:
Defining cell state and type without calculating distances in expression space
Usually, cell types are found by clustering cells in expression space (or some lower dim. projection of it), and calculating differentially expressed (DE) genes. These DE genes are then used to annotate the cluster to a particular type. Cell states are then thought of as a 'fine-grained' view on this cluster, making some reference to a biological process.
However, this means that a particular cell state can never be present across cell types, whereas we do think of them like this. For example, "being at a certain point along the cell cycle" can be thought of as a state, or "being under stress", and cells of different types can be in these states simultaneously. Is there some principled way to extract such states from single cell gene-expression data? It should be able to annotate different, far removed regions in expression space as being in the same state, so probably cannot be based on distances in expression space.

It kind of sounds to me like you're thinking only like a computer scientist and not like a biologist. If you want to know where a cell is in the fell cycle, consider looking at cell-cycle related genes. If you want to look at stress, look for expression of stress-associated genes.

That is true, I am approaching this as more of a computational problem. That said, I think there would be added value in being able to detect novel states, not just ones for which you know a set of marker genes. For example, there might be a state defined by three genes (A, B, C) being expressed together. It could be the case that these three are only expressed together in distinct but disjoint locations in expression space. I was wondering if there are known methods/algorithms for detecting such states.

I would expect that the kind of correlation structure that you describe would be amenable to multivariate analysis. As a very simple-minded approach, you would expect that PCA would find a projection in which (A, B, C) are all strongly loaded and other genes are at the noise level if their signal is strong enough and your data are properly normalized (how to normalize is a separate question), even in the presence of other large expression signals like cell cycle etc. Can you add more specifics about what exactly you have tried?

My suggestion is that you rethink the premise of your question. Projections and distance comparisons can be used to define cell states that apply to multiple cell types.
Here is an example. A and B are two cell types. S and T are two cell states. x and y are two genes used to define these states. The plot below shows expression of gene x on the x-axis and gene y on the y-axis. The vertical line separates cell types. The horizontal line separates cell states.
                gene y
                ^
                |
    state: S    |    state: S
    type:  A    |    type : B
                |
<==============================> gene x
                |
    state: T    |    state: T
    type:  A    |    type : B
                |

Thanks! This is a very useful diagram, and indeed how I had been thinking about it. I've accepted your answer as I think it illustrates the point nicely.


text:
Ischemia-induced deploarization in excitable cells
I have read in many sources that ischemia-induced depolarization is due to the opening of ATP-sensitive potassium channels and inactivation of Na/K exchangers [1,2]. However, K-atp channels are inward-rectifiers and their extensive opening should cause extracellular hypokalemia besides the fact that in low [ATP]i during ischemia, Mg++ ions are free (not complexed with ATP), and magnesium ions are outward potassium current blockers (i,e, they increase the rectifying power of k-atp, Kir, K-Ach channels)[3,4]. this would cause extracellular hypokalemic depolarization. What is the source of hyperkalemia then?

Inward-rectifying means positive current passes more easily in the inward direction, however it won't flow differently than the membrane voltage and reversal potential dictate. See for example https://en.m.wikipedia.org/wiki/Inward-rectifier_potassium_channel
The only time you'll have potassium flowing in to a cell, rather than out, is if the cell is very hyperpolarized, beyond the reversal potential for potassium, which is more negative than the resting potential.
Open potassium channels will almost always reduce intracellular potassium concentration as potassium flows out of the cell. Without ATP to fuel the sodium-potassium pump, there's no way to restore the lost potassium.
The existence of a negative resting membrane potential is due to relative concentrations of potassium (high inside cells) and the existence of primarily potassium conductance in the membrane, which means a few positive ions leak out to make the inside negative. If you don't maintain that concentration gradient, the cell is going to depolarize.

I'd also suggest an honorable mention of the chloride anions that stayed within the membrane in the last graph.

i will try to explain what i understood. So, when the K+ channels open during repolarization the permeability is so high that according to goldmann's equation the resting membrane potential (RMP) is closer to K+ reversal potential(hyperpolarization) But as repolarization ends the fast and slow rectifyer channels close so the RMP shifts to a more positive voltage and then K-leak channels and K1 (inward rectifyer) channels open and since they are not as abunduntly opened as the channels during repolarization.........

..... the RMP is still more positive than it was at end of repolarization. this causes the correction of RMP to the pre-depolarization state. So the main function of K1 is to allow rapid influx of k+ ions to correct hyperpolarization as fast as possible and thne k+ leak channels maintain their efflux. Am I right?

@kljiuklk1 Unless the membrane voltage is more negative than the potassium reversal potential (which can never happen by potassium flowing alone, no matter what channels are open), potassium net flow is always out of the cell. There's no "rapid influx of potassium ions". Leak channels are always open. Recovery from hyperpolarization happens because other ions (mostly sodium) are leaking in faster than potassium is leaking out.

@BryanKrause, but if that is the case then why the correction of hyperpolarization is attributed to K1 channels. And why would there be an inward rectifyer if potassium is always flowing out even at hyperpolarized state?

@kljiuklk1 Mostly those channels can be thought of to be somewhat self-closing when cells depolarize, which allows for cells to both have more "leak-like" current at rest, making them less susceptible to "accidental"/random depolarizing events, yet not interfere with the depolarizing current which is metabolically costly if you have lots of sodium and potassium flowing against each other.

It's somewhat random luck that at severely hyperpolarized potentials those channels are even more conductive, but those conditions only occur artificially.

Note also that "inward-rectifying" is just the direction of the rectification... The function continues in that direction within the physiological range where potassium is always flowing out, it's just that there is a higher conductance when closer to rest and lower conductance when further depolarized.

I cannot think of a non-artificial circumstance in which a typical neuron or muscle cell would have a potential more negative than potassium reversal. Im not sure where you've gotten the idea that they are responsible for "correction of hyperpolarization" outside of artificial circumstances.

so if i understand correctly inward-rectifier is another way of saying weak (semi-closed on efflux) K+ channels (i,e, it allows the membrane to reach the point of RMP according to goldmann equation but at less permeabilty and slow rate (slow K+ efflux) ). If we were to remove the rectifier function of these channels, the RMP will decrease because non-rectifier channel is more permeable to K+efflux .right?

@kljiuklk1 I wouldn't think of them as weak, either, actually I don't know what their overall single channel conductance is, but it need not related to the presence of rectification. Rectifying is a relative thing. It's mainly that they are just most permeable closer to resting potential, so they help maintain resting potential without interfering with spikes as much.

So, inward rectification is just an identification property rather than a functional property (at normal physiological level) and if inward-rectification of a channel increases this means in the other way around that outward-rectification K+ effllux decreased and thus its conductance decreases. as inward rectification can be increased by increasing [Mg]i which according to some research blocks the outward-rectifier portion of the gate and thus the cell will b emore depolarized.

@kljiuklk1 No. I'm sorry, my patience for this has run out. Read to what I am writing, read about these channels in more than one reputable source, and don't keep trying to add on your own meaning to things or inventing terms like "outward rectification decreased". Channels are what channels are. If you lose potassium channels, of any type that have any open probability at rest, the resting potential will be less negative. You can test this out using the Goldman equation.


text:
Do complementary DNA sequences/codons produce the same amino acids?
I haven’t been able to confirm this anywhere. If this were not the case, when transcription occurred, if the transcription were based upon the incorrect side of the DNA molecule, a completely incorrect output would result. Complementary sides should be aliases of each other, but I have not been able to find anywhere whether this is the case.

Isn't this trivial to answer using a chart of the genetic code? How do you think transcription would start on the "wrong" side?

Welcome to the site. Please take a [tour] and visit the [help] to find information on what we do here. In particular pay attention to the homework policy, which would cover your question. You could self-answer your question by thinking about strandedness and direction of transcription!

@BryanKrause In the very least, in this image, the sequence UUU does not produce the same results as AAA: https://ars.els-cdn.com/content/image/3-s2.0-B9780128008836000112-f11-05-9780128008836.jpg

“Complementary sides should be aliases of each other” — are you assuming that complementary strands should produce the same proteins when transcribed and translated? Why do you believe this to be true?

If DNA intends to code for one set of amino acids, would it not be wrong for a ribosome to build a polypeptide from different amino acids than one side of the DNA molecule intended for? Essentially, if one side of the DNA molecule depends on the other side of the DNA molecule, why would it ever be the case that complementary sequences don’t produce the same amino acid outputs? Since DNA is symmetric, I don’t see how the ribosome would be able to determine which side is intended to hold the information, in the case that complementary bases within codons don’t code for the same bases.

@acvill Does the whole “DNA transcription to RNA to translation within the Ribosome” process have some way of determining which side of the DNA molecule was supposed to be read? Since DNA is supposed to be complementary throughout, if I wanted to store some sequence on one side, I wouldn’t be able to just continue on storing more information on the other side of the molecule- the other side would be reserved for a chemical mirror image of my stored information. If one side holds the desired code and the other simply holds the backup copy, I only intend for the desired side to be read- but how?

Transcription is a highly regulated process, cells aren't just producing random RNAs from random stretches of DNA.
The transcription machinery needs to bind to DNA to get started, which requires a promotor sequence. It's not necessary for DNA to "read" the same way forwards and back, because it'll only be transcribed in the correct direction.

My question is not about the direction of transcription and translation, but rather, which side of the molecule the process begins copying from (i.e. not along the molecule, but across to the mirror side). If one side’s sequence deterministically depends on the other’s, is it the case that either side (i.e. codons containing exactly complementary bases) would produce the same output? If not, then why? Is there some way of ensuring that only one side of the mirrored DNA structure is read?

Yes, only that side "fits". DNA is directional (the ends are referred to as 5' and 3' ends). If you read the whole Wikipedia page on transcription or an equivalent chapter in a biology textbook I think it'll become clear. If you wanted to transcribe the other side, you'd have to start at the "end" and work backwards.

Thank you. I think this directionality shows me where the cracks of my question lies.


text:
How likely is rabies virus will enter the body through this kind of imperfect human part when you perform this "experiment"?
First, let's not confuse my question with typical skin peel when your body part slip on a road and get that typical red colored skin due to blood. It's not like blood is flowing, but clearly red area is visible due to some upper skin damage. This often happen when you fall from motorcycle and friction between your body part and the road (especially when you're not wearing riding gear).
Example
I read somewhere that skin abrasion is considered open wound which definitely can cause rabies spread if it came in contact with virus.

My question is more about non bloody/reddish skin imperfection of any human body part for some reason. The similar peeling can occur for many other reasons. E.g. when hands or even toes have been wet for long time then the palm or finger tips, toe skin is more likely to peel if someone manually tried to peel it.
Important thing is - it usually doesn't cause any noticeable pain or blood.
Here is an example that will clarify a little:
Example
It's like the skin is peeled (manually or through some disease). There's no blood though as upper layer usually doesn't cause pain.
But unlike this palm skin if someone tries to peel the opposite side of their palm (I mean the skin where there are hairs on skin i.e., the back side of hand), it is more likely to give pain and cause red area/blood.
So the focus of my question is around an imperfection of a skin which doesn't have blood and pain.

Here's the thing I'm curious about:
Suppose a dog has rabies virus in its saliva. And we collect the sample in a glass. And then make a contact (like submerging for few minutes) with the saliva with the human part.
In simple terms, that particular part of human body has touched that saliva.
Now I'm interested in knowing how likely is rabies virus will enter the body through this kind of imperfect human part when you perform this "experiment"?

Why am I interested in knowing this?
I belong to a developing country where education system is not good enough. So you can't expect a college professor in average college to answer you about this. And top colleges need high skills. I want to educate myself and people around me. Most people around me know that you can get rabies only when a dog bites you and a lot of blood is flowing. Which I think misses a lot of information or it is incomplete.

What I've studied so far is this:

Rabies virus can spread through bites (which is easy to understand because wound is deep)

It can spread through wounds which are deep or at least have blood (I'm really not sure if my example is considered a wound or not )

Saliva of a dog will contain the rabies virus after the incubation
period (read here) But in my question, let's assume dog saliva
contains the rabies virus

Example of a few skin problems I read here: https://www.healthline.com/health/skin-peeling-on-hands (I could not add it to my question because it was marking it spam)

You asked this question a few months back. This is a medical question, as it concerns your skin lesions. We cannot predict how likely it is in every situation; strange things can happen, but usually don’t. How likely is it that someone will be killed by a stone gargoyle breaking loose from an old building a moment before they walk by? Highly unlikely but it has happened. The CDC has a lot of good information on rabies which might reassure you. No one, though, can predict with any accuracy a one-off event.

@anongoodnurse where did I say "my skin" or "your skin"? If someone asks a question about skin, human gut, immune system, cell, human muscle, baldness, retina etc. (which of course are posted here usually) that doesn't make it "my" or "your" body part. It's a general question.

Secondly, I tried my best to edit this question after moderators and others suggested me to edit it. I might have not done better editing but I still think it's definitely not asking for personal medical advice now.

If we were not aware of your previous question, the present question (which contains long passages verbatim from the personal medical question you asked), maybe this would “fly”.  However, the problem exists that this is a thinly veiled personal medical question. At least you have your answer.

@anongoodnurse okay. The thing is I did not try to hide my past history. It's public. But I really don't think dragging my past history into this separate question to prove it a personal medical question is a "Be nice be respectful policy". That is what close votes and down votes are for.
And why do you think there haven't been many personal medical questions already haven't "flown"? Or won't fly in the future?
Irrespective of the past, my whole intention was to get educated and educate people around me on this topic.

There is a whole lot of difference between developed countries and developing countries about rabies. People here aren't aware of many basic things about rabies. People "assume" a lot of things without facts.

If asking this question helps to gain knowledge to someone, I really don't think it's a bad thing.

One thing I would point out is that no one in their right mind would collect the saliva of a rabid dog then submerge their broken skin into it. So what, exactly, are you educating the public about? Have you seen this done? Have you tried to talk people out of this? The answer given, which is rock-solid, concerns people who have come into contact with dogs they have assumed to be a non-risk for rabies, and paid the ultimate price for their mistake. The scenario you propose is unfathomable…

…and if it leads you to try to spread false information about the risk of rabies from objects in the environment, that is not educational, it’s the opposite: it’s misinformation. There are orders of magnitude between the solid answer and the risk of contracting rabies from an object outside where a rabid dog may have wandered .

@anongoodnurse that is the worst argument. If you think everything could and should be prevented only when it realistically happen, that isn't how someone educated always. Prevention is better than cure and there's a far big difference of importance between experiment and accident. I am not spreading false information, you are trying to prove my question is far worse than actually it is.

Your logic is worse. It is like blaming Louis Pasteur too by trying to experiment to find cure rather than naturally waiting and getting infected by rabies and then find a cure.

Finally, I never tried to spread false information. I tried to investigate facts. Do you see difference? Please read my old history and this question again. You're stuck with my old history. There's no point in argument. I rest my case.

I don't think anyone can give a good estimate for the risk from such exposure, but it is not zero. From “Scratches/Abrasions without Bleeding” Cause Rabies: A 7 Years Rabies Death Review from Medical College Shimla, Himachal Pradesh, India:

We investigated 19 deaths due to rabies in the past 7-year period. Of these, five were caused by “scratches/abrasions without any bleeding” and no postexposure prophylaxis (PEP) was sought. All injuries were caused either by unvaccinated pups below 3 months of age or by stray unvaccinated dogs. Four deaths were of patients who received proper wound care along with minimum 3 doses of intramuscular rabies vaccination, but rabies immunoglobulins (RIG) were not given or were not available. In eight cases, no PEP was sought as the patients were either not aware of its need or the PEP facility was far away or the PEP cost was not affordable or deceased believed that pups below 3 months of age do not carry a risk of rabies. In one case, the patient was bitten by a cat 2 years back. Majority patients belonged to rural and remote areas. Five of the deaths in our study were because of not seeking prophylaxis as abrasions/scratches without bleeding were not thought to carry a risk of rabies. In the Philippines, a rabies death review of 1839 patients demonstrates that all deaths were due to dog related injuries including bites and scratches.1 In Iran[2] four people having scratches on their hands were infected with the saliva of rabid animals and died due to rabies, there was no history of bites. In our death review also, deaths caused by “scratches/abrasions without blood” amply demonstrate the ability of the rabies virus to enter nerves through dermis due to broken skin and its capacity to cause rabies.

So, clearly, bleeding at least is not necessary for infection. My guess would be that many skin conditions would provide the virus enough access to susceptible cells that infection could result. Personally I would seek treatment after any exposure to potentially infected saliva, even on completely healthy skin.

Thanks. That is helpful information. I wonder why some users are reluctant on sharing information on this topic. I know it's not easy to answer but not every answer needs exact and 100% fool proof facts right?


text:
Fresh Water Fish Identification
A couple of days ago I just adopted a group of 7 fishes, 2 inches long each, orange-pinkish color, a black dot before the tail, very fast, active and peacefull. Looks like a kind of tetra fish. Anyone?

Some kind of barb.

Could well be the Rosy Barb, which is a common beginner fish (I believe, not being an owner of a tank at all).
They have a distinctive reddish colouration which is brightest when in the mating season, but otherwise much paler. Their scales seem to be slightly iridescent and they have a black dot at the base of the tail. The males have black tips to the fins, but the females do not have the black tips.


text:
Are there any bacteria that could be used as food?
Bacteria are found everywhere. They can also grow on various substrates. Are there any bacteria that can be used as a food source? For example mix x with water and add some of these bacteria. These then either turn x into something nutritious or can be consumed themself. Are there any potential candidates? Bonus points if the substrate bacteria use to grow is abundant.

I think the catch might be nutritional density. Remember what happens when bacteria get too concentrated in brewing: They die out like in brewing alcohol.

Does yogurt count? Beer? Other fermented foods?

I was rather thinking about something abundant but not nutritious themself.Are there any examples with wood / cellulose?

https://en.wikipedia.org/wiki/List_of_microorganisms_used_in_food_and_beverage_preparation

@DKNguyen The die-off in uncontrolled beer fermentation is due to the alcohol produced by Saccharomyces cerevisiae, which is a yeast, not a bacteria.

One more fermented probiotic product https://en.wikipedia.org/wiki/Kombucha Though whether it is actually beneficial, is unknown, there are different opinions on that.

The best example of bacteria-as-food is the genus Arthrospira, which is a kind of cyanobacteria whose edible biomass is known as spirulina.

I didn't realize algae were classified as bacteria.

@DKNguyen Somewhat confusingly, cyanobacteria are both known as "blue-green algae" and also not really considered algae. Algae in general as a term is highly non-specific.

If consuming spirulina, note that spirulina can be easily contaminated with other algae's toxins, and that spirulina should be avoided as a vitamin B12 source as its B12 bioavailability is questionable.

From the comments:

I was rather thinking about something abundant but not nutritious themself. Are there any examples with wood / cellulose?

In fact, the traditional Filipino food called nata (examples of which include nata de coco and nata de piña) are basically cellulosic pellicles of the bacterium Komagataeibacter xylinus, produced by culturing the bacterium in the appropriate medium (coconut water for the former, and pineapple juice for the latter).
(This resembles the SCOBY that is used in making kombucha.)

While not used as a food per se, bacteria are used in production of many foods, and you eat masses of them when consuming the product. At a guess; in the 10's of millions per bite is my estimate.
One type that is commonly used in several sorts of foods are the Lactobacilli. These are commonly used to generate sour products, through their fermentation of sugars into lactic acid. They are used extensively in yogurt production (Lactobacillus acidophilus usually), as well as other fermented diary products (cheese, kefir, cream cheese, sour cream, etc.) sourdough breads, production of fermented pickles such as sauerkraut and kimchi.
In some cases, such as kimchi and sourdough, these are often the natural lactobacilli and other bacteria and yeasts that are on the material used to make the product, so no added culture. In the case of sourdough, the fermentation can also be a result of yeasts in addition to the lactobacilli.
Similarly, acetic acid bacteria (Acetobacteraceae) are used in the production of vinegars, though in most cases these are filtered out before selling, so you don't generally consume them.

Apart from the classical microbial food processes, there is also a more recent approach captured under the term "single cell protein" (https://en.wikipedia.org/wiki/Single-cell_protein). Basically microorganisms are grown on a suitable substrate, and the protein that makes up their cells is used as food. Typically it would be either a food supplement or used in animal feed.
Regarding bacteria, it's most interesting to look into autotrophs, which can fix carbon from CO2 with a source of energy, or methanotrophs, which grow on methane derived from natural gas or biogas.

Additionally, there are efforts to use methylotrophic (which eat methanol or methane) organisms as sources for protein. In the future this might be particularly interesting because methanol and methane can be produced renewably from CO2, water and renewable energy. See e.g. https://solarfoods.com/ (I'm not affiliated with them).

Basically all the mammals which eat a diet comprising hard-to-digest plants like grass, scrub, etc. use bacteria exactly like this. So cows, horses, deer, camels, goats, koalas, and so on. They either use foregut fermentation (like cows) or hindgut fermentation (like horses). In either case microbes, including bacteria, break down hard-to-digest carbohydrates like cellulose into easy-to-digest simple sugars.
For some foregut fermenters like ruminants (e.g. cattle), gut microbes (including bacteria) are also an important protein source--the cow gut is split up into multiple sections, the first section (the rumen) is a comfortable place for microbes to live and break down cellulose but some of the microbes end up traveling with the food into another section where the microbes themselves are also directly digested by the cow.
Even humans have some bacteria which do this in a limited fashion, just not as efficiently as grazing animals.
Bonus side note: This does not include panda bears. Panda bears eat specific parts of bamboo which are easy to digest and high in protein already and their digestion functions much more like that of a carnivore.


text:
Why are DNA samples stored as biochemical samples and not as binary data?
Why are DNA samples stored in cryogenic conditions as biological (or bio-chemical) samples and not as binary data streams of nucleotide sequences in a hard disk or tape drive?
A few reasons I can hazard a guess at are -

Cost to sequence
Cost of data storage (?)
Reliability  of sequencing?

Is there any motivation - financial or academic to achieve this?

I think it would be really useful if you gave more information about specifically what DNA samples you are talking about and why you think they’re stored cryogenically rather than as sequence data.

@user438383 - I was thinking of the 23&me kind of services and forensic evidence. A DNA of a fugitive can be made available worldwide and matched with active investigations across borders if the DNA were in digital form.

@LordLoh.  23&me does not fully sequence their customer's DNA. Rather they sample some important spots that are known to be informative, and check those sequences. DNA identification for law enforcement generally doesn't using sequencing at all. They rely on  a technology called DNA Fingerprinting. Law enforcement has to hang on to samples so that the defense can examine them with their own experts.

One reason DNA samples are kept is because we might want to do further analysis using them. If we relied on digital records we'd have to synthesize  the physical DNA from the digital record, adding an additional step and possibly introducing errors.
The larger reason is that DNA is not a digital code, it's a large, complex molecule. It happens that many important properties of DNA can be modeled as a simple digital code using the sequence of the four bases, but this is by no means the whole story. For example, in cells with nuclei, the DNA is wound around complex protein structures called histones. The histones in turn can have subtle chemical modifications that have profound influences on whether the DNA wrapped around them is active or not. Furthermore the DNA itself is subject to chemical modifications that aren't usually noted in the standard genetic code. The most important of these is DNA methylation, which again is critical in determining the activity of a region of DNA.
Many people spend their entire careers studying DNA via data streams of nucleotide sequences on computers, but when you have new insights, you often want to test them in a wet lab using physical DNA.

It's also most common to store DNA not as a molecule but as part of an organism that contains all the machinery to make more DNA (and everything else) when you need it; spores, cells, seeds, eggs.

It’s also often not trivial to just synthesize DNA whenever you need it, and this is especially true for larger sequences. Even for something small like an expression vector, one would typically have only the insert synthesized and then subclone and transform it into some organism. All this takes time and money.

The answer by Charles Grant is absolutely correct, especially with respect to our limitations with sequencing DNA of biological origin.
I'd like to add that DNA is also a much more stable storage medium than digital storage. DNA can effectively retain encoded data for at least 2000 years and can still produce living organisms after >30,000 years. Digital storage becomes corrupted within several decades.
DNA also has an extremely high information storage density, and there have been several efforts at encoding digital data as DNA.


text:
Is this Poison Hemlock?
There is a lot of this growing in standing water near a drainage route and spring. It looks similar to water or poison hemlock.

This is most likely water cress (Nasturtium officinale), which is in the cabbage family (Brassicaceae).
This is a water dwelling species that has white flowers and leaves in a pinnately compound form and flowers in clusters.
In contrast, hemlock (Conium maculatum) has its flowers in distinct umbels (umbrella shape), and the leaves are also pinnate, but deeply divided and lacy in appearance as opposed to the intact and lightly toothed edges on watercress.
Here's a picture of hemlock leaf from Iowa State University, contrast it to the ones in your question:

Thanks! It looked similar but is missing distinguishing features like umbels, 5 petals, reddish stem, protruding stamen, etc.

@noshery no problem, it is certainly good to get clarification around these sorts of things. Water cress is very edible and tasty, though rather peppery when raw - tastes like radish or mustard. If you are certain that the water source is clean (i.e. not polluted or have human/animal waste in it), then harvesting and eating is a possibility, but could need cooking if in doubt as to the water.


text:
What is this marine creature? Is this a fossil?
Found this on a beach on the East coast of India - Vishakhapatnam, India
Is this a fossil? A coral?

Its small enough to fit in my hand

These tunnel-like structures are hard like rock/calcified

Obverse

Obverse

Doesn't look like a fossil because doesn't look rock-like enough and not buried. Maybe this? https://gohiking.ca/animals/fish/marine-worms/calcareous-tube-worm/

Its not a fossil.
It is just shells of various marine invertebrates that get stuck together as they grow. It looks like worm-snails on a a large piece of clam shell. the little holes in the clam shell are bored by sea snails and erosion.

there are whole blogs devoted to finding interesting examples. https://natureinfocus.blog/2010/01/13/calcareous-worm-tubes-on-flat-oyster-shells/


text:
What is the bird that are on house and make sound during part of the night?
For a few weeks, my neighbour is disturbed by a sound that seems to comes from me. It's mostly heard at the end of a day, but he said the sound stops in the night.
After checking, yes, it seems to be in multiple houses, but comes from the top of house. The sound stops when we are very near it (like 3-5 meters).
I tried to show them, like check if I can see some part of bird, but nothing.
I made few recordings. WARNING: all record are very low in sound, can't do better yet. Sorry for the noise. They are all hosted by discord.
Latest sound that seems not so bad: here (doesn't require download)
Record that require download:

First sound
Second sound

Doesn't require download:

Third sound
Third sound but with noise removed

Do you know what are those things and how to prevent them? Do you need more things to identify them?
External information:

I'm in the middle of France.
All sounds have been recorded today.

Much better, I'll leave it to the experts who can tell and delete my old comments now.

Have you tried https://www.chant-oiseaux.fr/ by chance? There are a lot of bird sounds there, and you may be able to find it.

I'd start with common baby birds - Common Starling (Sturnus vulgaris) is a likely target as is black bird (Turdus merula).


text:
What is the relationship between stress granules and circular RNAs?
I have read that circRNAs act as sponges for miRNAs and that stress granules help reduce chronic cellular stress and they are composed of proteins and RNAs. I'm interested in the relationship between these two phenomena in Alzheimer's disease. They both seem to be important to mark the disease and there is possible evidence of circRNAs in stress granules.
Is there a specific relation between the two? I would like to know even if it doesn't actually relate to the disease or not.

Can you cite/link the references that you have read that state this?

Stress Granules source : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4256948/

Circular RNAs source: https://pubmed.ncbi.nlm.nih.gov/30259371/

I've added these citations as links, as well as a potentially useful citation for the relationship to Alzheimer's.

Thanks! That link is pretty useful.


text:
When to use fixed effects vs random effects models?
I had previously read some on this topic and my understanding was that a fixed-effect model is when you are sampling an entire population, for example, a school district, a school, or a village. And a random-effects model would be used when taking from any of the populations a sample where the goal of the random-effects model would be to estimate the population. I am reading Successful hunting increases testosterone and cortisol in a subsistence population and the authors describe:

Individuals were modelled as random effects to control for
non-independence of multiple specimens collected from the same
participant.

I am not understanding this that well and am asking for further explanation, please. While on the one hand, it seems because the entire population (viz. the village) was not sampled we would use the random-effects model.

Is there some reason you aren't asking this on [Statistics.SE]? If not, I recommend you move the non-biology questions to that site and delete them from this one; NB: please do not crosspost. ——— Please also post each question separately — this helps you get answers to each question and makes those answers much easier to find for future users. Please see the [tour] and consult the [help] starting with [ask] for details.

@Tyersome IMO this is a good fit for the site. It's contextualising a statistical question in terms of biology - the biology is key to the question.

There are too many questions here; I've removed the additional questions, but you can ask them separately.

For the quoted text, the mixed vs. fixed has nothing to do with sampling the entire population vs. a subset but rather with multiple samples per individual. This makes the samples non-independent, so a mixed model is necessary. The question is better answered here: https://stats.stackexchange.com/questions/4700/what-is-the-difference-between-fixed-effect-random-effect-and-mixed-effect-mode

While I am a biologist by trade, not a statistician, I still do a fair bit of statistical modeling. It seems like you were taught a flawed, or at least incomplete understanding of mixed effects modeling. While your experimental design is what determines whether an effect is fixed or random (at least it should be), the description you gave doesn't really match with how they are used (at least in my experience with modeling). I'll try to break that statement down a bit just based on what you wrote in the question.

... my understanding was that a fixed-effect model is when you are sampling an entire population, for example, a school district, a school, or a village. And a random-effects model would be used when taking from any of the populations a sample where the goal of the random-effects model would be to estimate the population.

First, you don't need to sample the entire population to measure a fixed effect. If you surveyed 10% of the people in a village at random, you still model your response variable as a fixed effect for that village. But, say instead you sampled 10% of the household units in a village, sampling each person within each household once. There are likely to be various environmental or genetic factors that are shared within a household that vary between different households. Because of that non-independence, each set of household samples can be thought of as it's own sub-population of samples that aren't truly independent from one another. So you would include a random effect term for households in your model, to account for those variations. But the actual response variable (or variables) of interest would still be modeled as fixed effects.
The same goes for the example in the paper. Even if the entire population had been sampled, each individual has their own unique set of genes and metabolic processes that can vary from person to person, so those repeated measures are not independent from one another. Modeling individuals as random effects allows you to see how your variables of interest are related at a population level without being confounded by those little difference between people.
This is one reason that cross-sectional study designs, where each subject is sampled only once, can be limited when it comes to generating generalizable inferences about a larger population. Without those longitudinal samples, it's not possible to account for any of that inter-individual variation in your models.
Mixed models can get pretty complex pretty easily with more comprehensive sampling efforts and study designs. Say you have longitudinal samples collected from multiple households across multiple villages. Now you have to consider how all of those confounding variables (village, household, individual) are related to one another and design statistical models in which each of those terms are appropriately nested to properly account for random effects.
For some more reading, I think this chapter from Applied Statistics for Experimental Biology by Jeffrey Walker does a pretty good job of explaining mixed how models work with some good examples of how they are constructed for different scenarios.

I think the confusion OP has about "sampling the whole population" should be about sampling the levels of factor, rather than the population. Generally, you use fixed effects when your data include all the levels of a factor (for example: Smokers and Non-Smokers cover everyone; smoking/non is a fixed effect), and random effects when they don't (for example, you sampled students in Paris, London, and Berlin; city is a random effect). However, that's not a comprehensive explanation of the difference, just a superficial guideline. It's certainly important for OP to learn more before using this.

(...cont) If you are "sampling each person within each household once" you don't need any random effects for the household - your error by household is wrapped up in your overall error term. However, if you sampled multiple people in each household, you may want a random effect of household to account for the part of the error that is shared among people in a household. It's only necessary when you have multiple observations there.

(...cont) Same thing at the village level: if you're sampling multiple villages, you'd probably have village as a random effect, not a fixed effect, if those villages are somewhat arbitrarily selected from all the possible villages in the world or in a country or whatever. If, however, you want to compare Springfield to Shelbyville as a research question, you'd model village as a fixed effect: you haven't chosen those villages randomly in that case, you've selected them specifically as part of your research question.


text:
What species of poplar tree is this?
I am looking for information on how to identify a poplar (Populus) tree. It is located in Dresden, Germany, next to a small stream. The city tree database lists it as Populus nigra. However, it appears different from other individuals of this species, and I have found inaccuracies in this database before, thus I do not trust it. In particular, the leaves are very large (I estimated ~15 cm) and firm.
There is an old individual (in rather bad shape) with furrowed "woven-looking" bark at the base, but turning smooth not much higher. This one is shown in the last photo below. There are several much younger individuals directly next to it, with smooth grey bark (see photo). Many of the leaves have some brown discolouration on the underside. Some of this can be seen in the photo below, although this leaf is cleaner than the rest.

I can take more photos of specific parts of the tree if this will help identification.

The Pl@ntNet app does not give any results with high confidence. Its best guess is Populus trichocarpa.

I think your conclusion of Populus nigra is correct. See for example this set of observations that only shows P. nigra and P. tremula observed in Dresden, and this set that only shows nine Populus species observed in Germany.
A good field guide, or better yet a "flora" (not sure the German translation, maybe pflanzenwelt?) of your area, or of Germany, should include a technical description of all the species expected to be found in the area.

First of all, thanks for taking the time to respond. This tree is in the city though, and there is no reason to think that it is native here. Many city trees aren't. I'm aware of which poplars are common here, but the very reason this caught my eye is that it looks clearly different from them. So I don't think iNaturalist observations are very relevant.


text:
Found this under a rock at the beach, removed it carefully and couldn't find any other bones, must be a marine mammal of some sort
Does anyone know what this is? I know this is not a land mammal because [details needed].

Unknown skull found under rock at beach.

No sign of eye sockets or jaw with teeth.

I have no idea what this is. Couldn't find any other bones.

How are you confident it is not a land mammal?  My first thought was a badger skull, but I do not think it is.

Perhaps a goat or sheep that has fallen of a cliff. The beach near me has lots of bones from farm animals who died from misadventure.

It's not fossilised either

you will not find eye sockets as you think of them in any marine mammal skull, the eye socket is mostly soft tissue.

A location in the world would be helpful for ID. Species present can vary widely depending on location.

A reasonable match for many features, bearing in mind the incompleteness of the skull is that of the South African Fur Seal (AKA. brown fur seal, Australian fur seal).:

Carolyn Stewardson, Tania Prvan, Meÿer MA, Raymond J Ritchie Copyright status unknown, fair usage via Researchgate
Shown here are views of an adult male of 10 years, the parts circled are those present in your specimen. The slight brow-ridge present on yours is just visible on the bottom plate.
The marked difference between your specimen and this one is the presence of sutures between parietal and frontal bones, which seem to be fused on yours indicating an older specimen (perhaps up to 30 years), but:

Suture age was not a good indicator of absolute age or age group

It's also difficult to tell the match of the slope of the skull bones away from the centre line particularly the parietal - which may be a match or not.
Submitted until a better match comes along.

Almost an exact match to the image, and the nuchal crest on the OP's skull is definitely that of a seal


text:
How to prepare ethanol-preserved insects for imaging using SEM
I have aquatic insect larvae (soft-bodied) currently preserved in 70% ethanol. I would like to image these using a scanning electron microscope (SEM). I am wondering whether I need to/can start at step 0/1 of the prepping process for the SEM or not:
Do I need to take my specimens out of ethanol, fix them using glutaraldehyde & buffer, wash them in the buffer and then return them to ethanol and dehydrate them with increasing ethanol concentrations?
Or is fixing not necessary for my specimens which are already in ethanol, and could I just increase the ethanol concentration stepwise going up directly from the current 70%?
I would appreciate any help!

This doesn’t answer your question, but I have some difficulty imagining that someone would give you access to their SEM without going over the various procedures with you. Have times changed so much since I used one in the 70s? Maybe SEMs are dirt cheap now?

I know what would normally be the required protocol, but I am not sure what to do because my specimens are different. Also the SEM I have access to is not usually used for biological specimens, so there isn't someone I could ask about the specific procedure in my case. If you have an idea I would appreciate the help!

If there’s no one to ask, I suggest you don’t try anything new. If your SEM isn’t set up for biological specimens, you probably don’t have the equipment necessary to prepare a specimen for a vacuum chamber. The specimen must be devoid of anything that might expand in a vacuum, and a special pressure chamber with the proper materials is needed to do that.

E.g. here. We had a small chamber and used liquid CO2 iirc as the final solution, which was then evaporated off in a vacuum chamber, then coated the specimen in gold. If you started with ethanol, I don’t think the final result will be of highest quality.

I will say that the final solution doesn’t need to be CO2. There are alternatives you can search for in google scholar. I found a paper that used 100% ethanol and let it air dry. But none that started with ethanol. Wish I had an answer, sorry. Also sorry for the tone of the first comment; it was uncalled for. You clearly know your way around a SEM.


text:
Why do you get dizzy when exhaling with resistance?
Why do you get dizzy when breathing out while something resists the air outflow and requires more pressure? Like when blowing up balloons or breathing out through a straw.
This even happens when breathing rhythm is relatively slow. That makes me wonder if the same physiological mechanisms are at play like with hyperventilating. The effect feels very similar at least. My impression is that something changes about lung functionality when it is subjected to higher pressure (in this case only during exhalation).

A major part of it is simply blood oxygenation (O2) and levels of carbon dioxide in circulation (CO2). Breathing rate and form determine these, and effects such as light-headedness and fatigue and blood pressure depend on them.
First... you get dizzy because you aren't getting enough oxygen. You need oxygen to function. This includes your vestibular system, which, when unoxygenated, makes you feel a sense of imbalance, or dizziness.
Second... CO2 reacts with the water in your blood to form the pH-lowering carbonic acid (H2CO3). In parallel, dissolved oxygen contributes somewhat to alkalinization (pH increase from baseline). When you hyperventilate as it works very much like "exhaling with resistance". In exhalations, lungs expel CO2 out from circulation. When you hyperventilate, or breathe more than necessary, you eliminate more CO2 than usual, which makes your blood more alkaline (incidentally this is why hyperventilating into a paper bag helps: the bag retains expelled CO2 you can breathe back in). More acidic blood can also lead to dizziness, which would be the case if you were not completing exhalations - or "exhaling with resistance"). Now, this explanation is a simplification, because blood has a buffer system that keeps pH steady. It's called the bicarbonate buffer system. In lieu of this, you'll find that you are more dizzy when bicarbonate levels are increased too, so it's not directly related with blood pH in the short term.
There are probably other contributing effects too. These are probably related to blood pressure (divergence from regular blood pressure, either hypo- or hypertension cause dizziness) as it relates to breathing pattern. This is because blood circulation and respiration are coupled in many ways.
Addendum: when you exhale but don't let the air out, it's called a Vasalva maneuver. It has physiological effects too, often short-term - grunting when lifting things is an example. You can read up on it too, it could be related to your query.


text:
Is there any evidence that physical appearance and temperament are coinherited together in humans?
Recently my wife and I had our second child, and I've noticed a trend with the two. Our first looks a lot like me, similar facial features and head shape, and along with it he also seems to hold many of my behavioral traits. Now with our second we're seeing the opposite, he looks a lot like mom (facial features and head shape) and so far he seems to have many of her behavioral traits, but none of mine.
My question is: have any studies discovered that appearance and temperament are (at least partially) inherited together? Has it been proven that a child who looks more like one parent, will likely behave more similarly to that parent?

Very interesting question, but I suspect the true answer is going to be exceptionally hard to find out. Disentangling the effects of shared environment and genetics on social traits in humans is a very very tricky problem.

No solid evidence as to linkage of appearance and personality traits, but there is some evidence of linkages of physical appearance and some medical aspects of health, e.g. cardiovascular fitness. But there’s plenty of evidence - solid - that many “personality traits” are heritable, and present from birth. I suspect it’s possible but not probable.

@user438383 anecdotal, but in my experience very specific traits are directly heritable - extraversion, memory capacity, language capacity, deductive ability. Essentially traits that are dictated by brain shape and structure.

When you say "in my experience" - do you mean in the twin-studies that you've read about?

Basic observation of parents/children, I've also got a bit of neurophys under my belt. I get that people at this stack won't like an unevidenced comment. The way I see it is that brain structure offers the basic framework, or template, for temperament. Environmental experience then interacts with that structure.


text:
Why is my tissue sample coagulating during centrifugation? How can I prevent this?
I am working on extracting water-soluble compounds from a biological tissue sample. A problem I am encountering is that the sample is too cloudy with debris/large tissue pieces to filter into HPLC vials for analysis. So my hypothesized solution is to centrifuge the samples and try filtering the supernatant instead.
When I tried this (centrifuging 5mL at 12000rpm for 5 minutes) the resulting sample was gelatinized/coagulated and even more resistant to filtration. Any ideas on why this is happening, centrifugation parameters to try instead?

What tissue are you working with, and how are you prepping it? If coagulation is an issue, adding heparin into your sample preparation procedure should inhibit it.

Welcome to the site, please take a [tour] and visit the [help] for information on what makes a good question and answers. To answer your question, as @MattDMo asked, we would need specifics on the tissue, reagents and procedures you are using in your preparation.  Also, besides centrifugation, what else have you attempted and how do others in your lab overcome this problem?

Your question and self-answer don't seem to make sense. You write about "platelet" in the question, but then say you were using plant-based samples in you answer. There is no point in posting publicly unless you are clear enough that someone else can learn from what you've posted. Consequently, I've voted to close this as "Needs details or clarity". Please follow the above advice and then either [edit] or delete these posts according to what you've learned (and whether you are willing to put the work in to improve your posts).

Answering my own question: I was using plant-based food samples that were extracted at medium/low temperatures. This denatured the proteins into absorbing more water. The samples were also starch-containing and gelatinized during centrifugation. I am only unsure why centrifuging initiates starch gelatinization like when cooking.


text:
Endosymbiosis Probability
What is the probability of endosymbiosis occurring? I remember seeing it in my AP Biology textbook but haven't been able to find it anywhere after forgetting it. I want to say I remember it being something like 1e-40 but can't say for sure. Also, I'm not a biology student so I'm not sure if endosymbiosis is the proper term for it but I think what I'm referring to is the successful absorption of a prokaryote by an organism to become a eukaryotic organism with mitochondrion.

According to endosymbiotic theory, the probability on Earth is 1. It's not really meaningful or useful to estimate probabilities of one seemingly unlikely thing that you have evidence has occurred. What do you hope to do with this probability?

You are going to want to look up endosymbiosis and algae for lots of examples of the spectrum of endosymbiosis .

I’m voting to close this question because it is unclear (or unanswerable due to not making sense), and lacks the expected level of prior research. Please note these are both sufficient reasons for downvoting and closure. Please [edit] your question and tell us: what your question is, where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.


text:
Can you identify this mosquitoe-like bug?
I'm wondering what is this bug, I have never seen it before and its behaviour is just weird for me, they just try to climb to the top of the window, then fall and start over again, I see no hole they are going through, they seem capable of flying but they don't.

(click to enlarge images)
Please help me know:
A) Which bug is it?
B) Is it harmful?
C) What business do they have with my window (What is attracting them?)
D) How do I get rid of them?
I'm in Mexico City and it was rainy up until this last days when they arrived, now it is warm, also I have some plants in the room but they don't seem to be interested to go near them.

Interestingly, one turned up on our kitchen table this afternoon. (Southern UK). Never knowingly seen one before. So, watching.

Unsure, but looks to be part of a mating swarm of ants. Not a problem if so.

Also unsure, but I think it's some kind of two-winged fly (Diptera); an in-focus photo showing wing venation would be a big help, but I suspect they're no longer around (it's been three weeks since this inquiry; the flight season for this critter might already be over).


text:
What is "Correlation of growth" according to Darwin and was he correct about it according to modern science?
What are the views that modern biologist have on Correlation of growth? I need some clarification on statement that I'm gonna mention below as well that is it reason to that as mentioned here: "The gradually increasing perfection of the human hand, and the commensurate adaptation of the feet for erect gait, have undoubtedly, by virtue of such correlation, reacted on other parts of the organism."
Quote mentioned above can be found here: Can be found here

@JiminyCricket. Sure, please find it here: https://www.marxists.org/archive/marx/works/1876/part-played-labour/index.htm

@JiminyCricket. Done !

I suggest that you look into spandrels.

[...] correlation of growth, as Darwin called it. This law states that the specialised forms of separate parts of an organic being are always bound up with certain forms of other parts that apparently have no connection with them. Thus all animals that have red blood cells without cell nuclei, and in which the head is attached to the first vertebra by means of a double articulation (condyles), also without exception possess lacteal glands for suckling their young. Similarly, cloven hoofs in mammals are regularly associated with the possession of a multiple stomach for rumination. Changes in certain forms involve changes in the form of other parts of the body, although we cannot explain the connection. Perfectly white cats with blue eyes are always, or almost always, deaf. The gradually increasing perfection of the human hand, and the commensurate adaptation of the feet for erect gait, have undoubtedly, by virtue of such correlation, reacted on other parts of the organism. However, this action has not as yet been sufficiently investigated for us to be able to do more here than to state the fact in general terms.

Much more important is the direct, demonstrable influence of the development of the hand on the rest of the organism. It has already been noted that our simian ancestors were gregarious; it is obviously impossible to seek the derivation of man, the most social of all animals, from non-gregarious immediate ancestors. Mastery over nature began with the development of the hand, with labour, and widened man’s horizon at every new advance. He was continually discovering new, hitherto unknown properties in natural objects. On the other hand, the development of labour necessarily helped to bring the members of society closer together by increasing cases of mutual support and joint activity, and by making clear the advantage of this joint activity to each individual. In short, men in the making arrived at the point where they had something to say to each other. Necessity created the organ; the undeveloped larynx of the ape was slowly but surely transformed by modulation to produce constantly more developed modulation, and the organs of the mouth gradually learned to pronounce one articulate sound after another.

First, the term correlation of growth is not often or frequently or widely used in biology. In my career I've know of no reference to it. That's why I preface with a comprehensive quotation to give readers a context of what is meant!
Second: if by correlation of growth, you mean that some trait is concomitant with another trait simply out of evolutionary contingency, then absolutely yes, modern biology would very much support this "correlation". However, it is stated above as a "law", and there exist countless instances in which traits are lost or gained in evolution. Mutations may produce gain- or loss-of function enzymes (genes), for instance. These enzymes possess chemistries hitherto unknown by the ancestral enzymes (genes) and so would violate a correlation with all other traits. It sounds more like a broad pattern or principle of thought than a biological law.
However, the idea that specialized traits are bundled together into organisms, and that organisms may only propagate into the future as lineages, is absolutely in line with modern biology. Thus, the expectation that unconnected traits, such as number of toes and number of ears, co-exist in a lineage for a while, is sound. It is also a little trivial too. At least for the vast majority of cases, in mammals*.
*Plasmid horizontal gene transfer in bacteria and other such things, again, would violate the notion that traits are "bundled" strictly within organisms and are only shared by descent... so I would rather mention that it'd be wiser not to think of it as law but rather as a matter of guiding principle.


text:
Is there any universally accepted definition for pain?
There are many terms in the literature of any domain of knowledge that does not have a standard or universally accepted definition. There can be several definitions from several organizations or textbooks. As a CS student, I am aware that there is no single definition for 'Artificial Intelligence.
I believe the same for the word 'pain' in biology. When I read about the opinions and research papers about 'pain in plants', I realized that some experts do believe that plants experience pain and others argue don't as they don't have any central nervous system. As a layman, I feel that pain can be subjective and pain for animals may not be apt to interpret pain experienced by plants.
Is there any universally accepted definition for pain in biology that encompass all living organisms?

“Pain in plants”? I remember someone in my university Philosophy Department who agonized about this. He left his wife and went to Australia. I’d check whether there is a more appropriate SE site for your question. There are medical yardsticks (I seem to remember childbirth scores high) but universally accepted biological definitions… I think not.

@David oh. I got the answer from you. If the question is not apt for this site. Please tell me. It is okay for me to remove it if needed.


text:
Finding population dynamics models for multi-generational species evolution with delays
I am working on a problem from economics, to understand how populations evolve within business organizations. I have found that some of the population dynamics literature is very relevant to my own work, but I am not very familiar with the vast biology and ecology literatures on this topic. I have been reading Murray's Mathematical Biology volume 1 bible, and it is really great--but it only gives a taste of the models out there.
I was hoping someone could help point me towards articles or models that deal with multi-generational evolution of a population with time delays. I have having a little trouble deciphering some of the biology or ecology terminology, so I am not sure if my search terms are correct--I have not been able to find anything like this, though I am certain it exists.
I am looking at a very simple model, something on the order of a system of differential equations with delays. So a simplified examples is below with just one species that matures over time. So for the same species, there are 3 populations, A, B, C, which represent stages in its lifecycle. I can refer to these in the model as $N_A, N_B, N_C$. Then there is a birth and death rate for each population, as well as a migration rate between the different populations--as individuals mature. I am thinking of the populations in continuous time, though of course suggestions for articles about discrete dynamics for such systems would also be valuable.
So the continuous system would be as below:
$$
\frac{dN_A}{dt} = \beta N_C - \gamma_A N_A - \nu_A N_A(t - \tau_A) \\
\frac{dN_B}{dt} = \nu_A N_A(t - \tau_A) - \gamma_B N_B - \nu_B N_B(t - \tau_B) \\
\frac{dN_C}{dt} = \nu_B N_B(t - \tau_B) - \gamma_C N_C \\
$$
So constants $\beta, \gamma, \nu, \tau$ represent constants for the birth rate, death rate, migration-maturation rate, and time lag. In my actual model I have 2 species that compete, but this model above gives a flavor of the dynamics. I would like to include some carrying capacity constraints too, but that can come later.
Like I said, it is easy enough to express this model in a discrete form as well. But I was hoping someone might be able to reference articles or something that shows someone analyzing discete multi-generational models--so that I can see a flavor of how they deal with the nondimensionalization, bifurcations, chaotic dynamics, etc.
I was hoping to see if other biologists or ecologists had studied this kind of continuous system, and how they had analyzed it. It seems like the first thing to do is nondimensionalize it, as I have way too many parameters. But I am not sure of a good scheme or equilibrium condition to use to do that.

"evolutionary game theory" plus "delay differential equation" (or "discrete lag") would be a good search terms to start with

e.g. https://scholar.google.ca/scholar?hl=en&as_sdt=0%2C31&q=%22evolutionary+game+theory%22+%22delay+differential+equation%22 .  Can you say more specifically what kind of  qualitative conclusions you want to draw (invasibility, evolutionary stable states, etc.) ?

@BenBolker Okay, I can start to search under these headings. I am seeing a lot of gene expression articles come up--can you tell me if gene expression models would apply here? Thanks for suggestions, at least I know I am starting to look in the correct places.

@BenBolker good question about what I am looking for. So I would like to understand if there are changes in the qualitative behavior of this system as I vary the parameters or move in and out of different parameter regimes. But right now there are like 9 parameters in the model. So I don't believe that I can explore the dynamics or find bifurcations without non-dimensionalizing the system or such to reduce the number of parameters. But yes, I would like to see if there are fixed points in the model, find bifurcations, any potential for chaos, etc.

Did you leave out a delay term in the final equation, i.e. should the first term on the RHS be $\nu_B N_B(t-\tau_B)$ ?

@BenBolker yes, you are correct. Thanks for pointing that out. I will update the OP.

You use the word "evolution" here to mean "change in populations over time", as is typical in (say) astrophysics (or, I guess, economics?). My initial comments and suggestions were based on a misreading of "evolution" having its biological meaning, i.e. change of genetic make-up of a population over time.
With that out of the way: delay differential equations are slightly less common than ordinary DEs in population biology, but still very common. I wouldn't say there are any special mathematical tricks that aren't also used by mathematical analysts or people studying dynamics in other fields ...

What you have appears to be a linear DDE, which is considerably simpler than the typical biological DDE, which will almost always have at least one bilinear term representing a species interaction (and often a stronger nonlinearity representing something like a saturating predator-prey functional response, see e.g. Chattopadhyay et al ref below). To be honest, I don't think that this system is going to admit any very bizarre behaviour, because of that linearity. The model is simple enough that it's possible that someone has actually analyzed this case ...
Fixed point analyses for DDEs are actually relatively simple, because when the system is at the fixed point the time delays are irrelevant (e.g. $N_A^* = N_A(t) = N_A(t-\tau_A)$) so your equilibrium equations simplify to (stars suppressed for laziness)

$$
\begin{split}
0 & = \beta N_C - (\gamma_A + \nu_A) N_A \\
0 & = \nu_A N_A - (\gamma_B + \nu_B) N_B \\
0 & = \nu_B N_B - \gamma_C N_C
\end{split}
$$
which is a pretty simple linear system, general solution shouldn't be bad at all. Stability of DDEs is harder, you'd have to look in a book ...

For bifurcation analyses, I think that standard numerical bifurcation analysis methods (continuation methods) can in principle handle DDEs as well, although to be honest I haven't checked them out -- some very basic notes here

You're right that a 9-dimensional parameter space is going to be hard to handle; in general you will only be able to get rid of two parameters by non-dimensionalizing (one for space/density and one for time). For the rest, you'll have to use the standard kinds of simplifications, e.g.

plausible symmetries/special cases

search the whole space over ranges that are physically/economically/biologically plausible

Here are a couple of fairly haphazardly chosen biological dynamics papers with DDEs:
Bonsall, M. B., S. M. Sait, and R. S. Hails. “Invasion and Dynamics of Covert Infection Strategies in Structured Insect-Pathogen Populations.” Journal of Animal Ecology 74, no. 3 (2005): 464–74.
Chattopadhyay, J., R. R. Sarkar, and A. el Abdllaoui. “A Delay Differential Equation Model on Harmful Algal Blooms in the Presence of Toxic Substances.” Mathematical Medicine and Biology: A Journal of the IMA 19, no. 2 (June 2002): 137–61. https://doi.org/10.1093/imammb/19.2.137.

Yes, thank you so much for the information it was very helpful. You certainly validated some of my intuitions, and also directed me towards the right places to look. I will read through the references you suggested. I will also think a bit more about the bilinear terms you mentioned. That is something that is still an open question and not yet resolved--but I understand what you mean, because this bilinear term occurs in the Lokta-Volterra equation or SIR models.

Also, the nondimensionalization information was really helpful. Many books emphasize those methods, but they seem to only work for small systems with a handful of parameters. I have had trouble finding any good references or treatments of how to reduce the dimension of the parameters. Like you said, I have seen cases where people use some conservation law or equilibrium condition for this, but have never found a good resource explaining the intuitions and ideas. I will check with a dynamicist friend, but if you have a suggestion, please pass it along.


text:
Terminology for Transgenes
I'm designing an in vivo delivery vector for therapeutic transgenes.
I have two different potential versions of the transgenes. If they were innate, they'd be referred to as "alleles." Does the terminology change if they're transgenes?

I think that "variant" would be pretty generally understandable. It might help to know what you mean by "versions". E.g. they homologous? How different are they?

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Yes, I would change to a different terminology. I would not apply the word 'allele', which would be confusing/misleading at best. Even if the transgene is an allele taken from an organism, I would only note such in a writing when needed and still refer to the transgenes themselves by something else.


text:
Are carrier proteins receptors?
I learnt about carrier proteins; how they bind a substrate/molecule, undergo a conformational change, and release the substrate/molecule on the other side of the membrane.
We can take Glucose transporters(GLUTs) as an example.
I see this "binding" to the carrier protein as something similar to how ligands interact with receptors. However, I don't know whether it is correct to classify carrier proteins as receptors.
Please help.

PS: Carrier proteins don't seem to fall into any of the types of receptors -- ionotropic, G-protein-coupled, or enzyme-linked.

Welcome to SE Biology. Please finish the [Tour] and the Help on asking questions to find out how this site operates. Specifically we expect posters to show that they have researched the question to try to find the answer themselves. If you search for "Receptor" in Wikipedia, taking the Biochemistry variety you will find how the term is used in biological science (rather than general English). Specifically it relates to signal transduction, answering your question in  the negative.

They are different molecules.
From Cell and Molecular Biology, Concepts and Experiments, 7th Ed., Karp"

Cells can only respond to a particular extracellular message if they express receptors that specifically recognize and bind that messenger molecule. The molecule that binds to the receptor is called a ligand. Different types of cells possess different complements of receptors, which allow them to respond to different extracellular messengers.

From Molecular Biology of the Cell, 5th Ed., Alberts:

Transporters (also called carriers, or permeases) bind the specific solute to be transported and undergo a series of conformational changes to transfer the bound solute across the membrane.

If one generalizes the definition, transporters may elicit signaling via indirect mechanisms, but the two classes are still distinct:

In contrast to bona fidae receptors, transporters and channels mediate the uptake of solutes, metabolites, drugs or ions, which themselves can act as molecular signals, once intracellularly accumulated.

The newly-identified transceptors possess both properties at the same time:

A relative newcomer in environment sensing are the so called transceptors, membrane proteins that possess both solute transport and receptor-like signaling activities.


text:
Why are additional classification levels necessary?
When I was in school I learned that all organisms can be classified using the seven levels kingdom, phylum, class, order, family, genus, species.  In the course of teaching my own children now, and in looking up information about animals with them, I find that there are additional levels like superorder and infraorder.
Is there a scientific reason why these levels were added?  Are the seven levels i learned insufficient?
I learned then with a lovely mnemonic, would be a shame to have to dispense with King Phillip and what he allegedly came over for...

What if you want to describe a group of organisms in between some of these arbitrary levels?

Relevant question on the usefulness of these designations: https://biology.stackexchange.com/a/55667/27148

It’s been my experience that these additional levels pop up when the more typical rankings are huge. For example, the family Asteraceae has so many genera that to even begin to work on the phylogeny of such genera without repeatedly listing dozens of names requires prior subgrouping of the family into subfamilies and tribes.


text:
What kind of scorpion is this?
This is in Nevada; it's about the size of a tooth pick in length.

(click to enlarge)
What kind of scorpion is this?

Welcome Samantha. Please take our [tour] and refer to thee [help] for guidance. I've edited to make the image work, which will apply once approved. Please tell us how big the toothpicks are in your part of the world as they vary quite a bit in size over the international community which visits here.


text:
Proof of shape of epithelia cells
In this article, the mentioned in the introduction that the  the optimal shape of epithelia cells in drosophila tissue is hexagonal (packing is approximately 6).
Is there an article that proves experimentally this shape? Or we just depend on mathematics and calculating the average neighbours?

Welcome to Biology StackExchange! I would suggest you add some references (or explain what you mean exactly) to your claim that the optimal shape is hexagonal. Firstly, there are several biophysical models for the shape of epithelia with varying levels of complexity. Secondly, the tiling is of course not hexagonal, it has to deviate to account for topology and cell division.

@Domen, I did. Actually I am coming from more physics background. Anyway, you said "several biophysical models". All these models are mentioning that the cells are taking a hexagonal shape (of course before rounding in cell division process). I didn't find something experimental I can fed from.

You might be missing the second part of the statement in the article: "The optimal cell shape on a flat surface is typically hexagonal as this minimizes surface tension". Therefore, the optimality in the simplest biophysical model is defined as the minimization of surface tension. Under the additional constraint that the cells be the same size, the resulting optimal tiling is the hexagonal one (compare with honeycomb). However, experimentally, we generally see that the tiling is not completely hexagonal, and thus this simple model does not adequateley describe the reality.


text:
How to Scale Metabolic rate and drug dosage according to Mass?
I was reading a book "Biology and evolution of Crocodilians" by Gordon Grigg and David Kirshner.
And I can't understand the part about metabolic scaling no matter which method I tried I can't get the same result as the one in the book.
(Box 1.2 and Box 7.1)
Box 1.2
It is about Lolong immobilization and dosage which has example of 0.5mg for 40kg Croc scaling to 2.4mg for 1075kg Lolong instead of 13mg, however no matter which method I tried I could not get the same number. (exponent for crocodilians is 0.829)
When I tried
(0.5/(40^0.829))×(1075^0.829) for Box 1.2 I got 7.65420145365 instead of 2.4
For Box 7.1
It gave example of 0.1kg to 10 kg mammal oxygen consumption scaling from 116ml/h in 0.1kg animals to 3483 in 10kg animals (as oppose to 11600 ml/h.) (exponent for mammals here use 0.738)
I tried (116/(0.1^0.738))×(10^0.738)
Which get 3471.02697847
Instead of 3483.
I have no background in science at all so it is likely I am doing something wrong.

Welcome user71055. We've an international community here many of whom simply won't have access to that particular textbook. Please quote the relevant text in the body of your question, then show what attempt you've  made to understand it (show your workings). Please also take our [tour] and refer to the [help] for guidance. Enjoy the site.

3471 and 3483 are the same number unless you have at least 3 significant digits of precision in all your estimates.

When I tried the
(0.5/(40^0.829))×(1075^0.829) for Box 1.2 I still can't get 2.4 but instead got 7.65420145365


text:
Is the microscope that gives these images considered professional?
I bought a digital microscope from Dinolite, model AM73915MZT, The use of the microscope is for industries like textiles and printing and graphics and for Ophthalmology / Iridology and Pathology [And as it says on the website that the manufacturer of this microscope is suitable for another wide range of applications].
As shown on the manufacturer's website here
The camera has a resolution of 5 Megapixel (2592x1944), and the sensor is of the CMOS type, with white LED lighting, including Polarizer.
The microscope costs $1469 before VAT and ancillary aids. From what I understand it is the best and most advanced model of this company.
I took some pictures with him, and at 220x magnification I can't get a sharp enough picture.
Attached an image of the calibration target provided by the company along with the microscope.
Image at a magnification of 220 - 10 barcodes

Image at magnification of 50 - 10 barcodes [marked with a red line]

You can see that the edges of the barcodes at magnification 220 times are not sharp compared to the edges at magnification 50 times.
Does this mean that the microscope is unprofessional or damaged and I need to replace it?
Is it related to Spherical aberration?
EDIT:

Both photos were taken with the microscope standing in the best stand of the company, model RK-10A.
If I rotate the adjustment knob slightly to
the right or left, the image only becomes more blurred, which means
that the position in the image is the maximum sharpness.
And for that I wonder if a microscope that this is its maximum sharpness - is considered professional.

EDIT 2:
Attached image of a scratch:
51x

228x

You can see that the 51x image is much sharper and crispier compared to the 228x image, does that mean that the microscope is neither high quality nor professional?
Razor
50x

229x

What microscope is "good" depends entirely on the application. "Professional" for what purpose? I don't think this site wants to get in to product reviews; these are typically off-topic across the whole SE network with a couple rare exceptions.

When I buy a camera I can see reviews on whether it is considered professional and whether it produces sharp and beautiful images, no matter what purpose I buy the camera for, is there no definition in the microscope for professional and good only in relation to the purpose?

For cameras "professional" also depends on purpose. This site is not for product reviews, for cameras nor for microscopes.

But as you stated, it's for textiles and other things unrelated to biology. Just because you intend to use it for biology doesn't make the question as written on-topic.

Professional is a marketing term. Equipment is not professional. People are. There are some instances where the stuff hobbiests use and make is more meticulous than that of paid professionals, because they can't afford to sit there and obsess. Just consider whether it's good enough and reliable enough for what you need it for.

Welcome to the site. For a good answer to this question, you need to provide some specifications on the lenses (type [e.g. plan, apo], f., NA.), camera (MP, CCD etc, plus settings [exposure, gain...], separate camera attachment or eyepiece?), microscope (compound, stereo, inverted, etc), and illumination type. Microscopes vary widely in quality and use-case and are not single instruments. Generally you need to pay $$$ for a good one. I routinely use microscopes with lenses that cost in the $4000 range for a single lens, let alone the rest of the 'scope.

@bob1 I added the details you mentioned, anything else?

Are you certain you have a blurry image of sharp barcodes and not a sharp image of blurry barcodes?

@timeskull What do you mean sharp image of blurry barcodes? If you look at the pixels of the image [for example at an 800% zoom in each image viewer] you will see that the blur structure is suitable for lack of focus - lens blur - and not for smeared ink and so on.

I don't know what technology is used to print the barcodes so I don't know what the edges will look like at high magnification. While I would expect them to be fuzzy, that's not necessarily the case. By my estimation the pixels in the barcodes of your top image are ~5.2 microns. Normal printers / normal paper cannot produce such small features.

@timeskull What do you think I need to photograph to be sure that if there is blurring it is because of the microscope and not from the observed object? By the way you can also see that the blur in all the barcodes is exactly the same, and as we would expect a blur caused by a lens.

you could just put a scratch in a glass slide and image that. If the edges of the scratch look sharp, then the calibration barcodes are blurry in reality. Otherwise, the optics of your microscope are the source of the blurriness.

@timeskull You can also look at the edge of a razor blade. Or a knife has been sharpened and honed by hand on a stone.

Basically you have bought a basic microscope that is not very good, with probably poor quality lenses and low manufacturing quality - the fact that they don't mention the lens manufacturer is a sign that has cheaper lens(es). A lack of reviews on microscopy sites also indicates that it is not well known. It may be suitable for basic hobbyist use-cases, and depending on what you want to do with it, it may suit you. Despite the blurb on the sales pages, no qualified lab would ever use something like this for pathology or any serious purpose; this is more of a toy than a microscope. Celestron has their "Handheld Digital Pro Microscope" that's very similar in specs to yours, but retails for about US$ 150 - just for some comparison from a manufacturer that has a good reputation for imaging equipment (telescopes in their case).
I don't think that it is broken, just that you have reached the limits of its magnification capability and if you were able to move it slightly closer or further away from the calibration you would get this in-focus. That it is out of focus indicates either that the stand is off by a bit (you definitely need a stand for that sort of magnification), or that the manufacturing of the microscope is slightly out. At 220x the engineering specs need to be pretty tight to get consistent focus. You won't get that sort of tolerance on a cheaper 'scope.
This is definitely not spherical aberration, as that would manifest as distortion of the image at the edges - a bit like a fish-eye effect. There will be some aberration in the lens (almost impossible to make one without), but this is probably corrected by a combination of software (like in your phone camera) and cropping of the image to only the centre of the image.
As you have brought it recently I would reach out to the supplier and see if you can get a replacement or a return/refund. If you have brought this for business use, get the company to fork out for a decent microscope brand - not only will they be more robust, they will give much better images and come with good technical support.
Good lenses and microscopes are very expensive and you only consistently get good lenses from well known manufacturers (Zeiss, Olympus, Nikon, Leica are the big names). There are some cheaper brands (e.g. Konus, Celestron [these two mostly known for telescopes], Saxon, AmScope)  that make some moderate quality microscopes for not too-high-a price (~$1,500) that make good basic microscopy starter packs. Second-hand microscopes are fairly common on re-selling sites such as eBay too, just make sure you get to see/use it before purchasing.
Without knowing your use-case I can't make any recommendations on what sort of microscope might be useful for you if you were to get a replacement, but your "classic lab microscope" is known as an Upright or Compound microscope, used for looking at small things up-close with transmitted light giving you a flat 2D image. You might be familiar with stereo-microscopes, which are commonly used for looking at large objects up-close in 3D, usually using reflected light. Stereo-microscopes are also often used for things like soldering electronics and manufacturing quality control in textiles.

Thanks, I read your answer and I think I missed important details about the stand in my question. I have now edited the question and added these details.

In that case, given those details, in the absence of vibration, the image is probably as sharp as it gets. As I mentioned in my answer, this is not a professional microscope - those cost much much more than you payed - a medium-high quality single-magnification objective lens costs about the price you payed for the whole set-up!


text:
Is this insect a bedbug?
I just found this bug on our bed. So even though it is literally a bedbug… is it actually a bedbug? We have never had an issue before and no signs of bites. But finding this worries me now…

Have you searched for pictures of bedbugs? Does yours look like any of them? What makes you think it might be a bedbug?

Yes, I’ve searched for pictures of bedbugs. As someone who isnt a bug expert — honestly, its hard to tell just by looking at pictures. I believe someone who knows bugs well would have an easier time identifying the pictures I submitted, which is why I asked.

Does this answer your question? This is a common question here.


text:
What is the difference between "ecological succession" and the term "stage of regeneration", is there a difference between them?
In ecology what is the meaning of the term "ecological succession" and the term "stage of regeneration", is there a difference between them?
Edit 1: Perhaps the term "Stage of ecological succession" is in English "ecological succession".

Where do you find the terms used? It's best to provide some context around questions asked here.

This term exists in Portuguese, I don't know if there is another term in English

Though this site is English-only, if you're taking something from Portuguese and taking a literal translation I think it's important to mention that in the question body. You're probably best off following citations in the Portuguese text to others in English, though.

Second other comments. It would be nice to know if you are talking about restoration ecology, forestry, disturbance ecology, or something else. "stage of regeneration" implies some of the above. There may be terminology that's specific to the field or the type of ecosystem.


text:
How do you do Polymerase Chain Reaction (PCR) if you don't have a thermal cycler?
PCR has three steps: Denaturation, Annealing, and Primer extension. Let's say you do not have a thermal cycler in the lab, how would you mimic similar conditions and perform PCR?

three water baths and patience

Worth noting that three reasonably accurate water baths might cost more (and definitely take up more space) than a small, cheap thermal cycler

Use of 3 water baths was the original method. Perhaps isothermal amplification an option? Many reagents change colour upon amplification to visually identify successful pcr, which could make screening faster.