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Protein - one polypeptide molecule or a collection of molecules?
I'm struggling a bit in Bio 111 with confusing terminology between the terms "chain" and "molecule". I understand the primary structure of a protein is a chain of amino acids connected by peptide (covalent) bonds - easily a molecule. And the secondary helix structure could be a single molecule/polypeptide chain. Up to this point, chain = molecule. But a beta-pleated secondary structure would have to be two or more chains (molecules) connected by hydrogen bonds. No? Or is a beta-pleated sheet considered one molecule? One chain?

beta pleats can still be a single chain and molecule, don't forget proteins fold which ba bring distant portion of the ame chain together.

Thanks John. But I think beta-pleated sheets must, by definition, be multiple molecules if you accept that a molecule is defined as consisting of only covalent bonds. I think I finally pieced the different terms together and cam up with definitions that work. I sure would like confirmation from anyone more knowledgable.

I think you are confused about what a beta-pleated sheet is, the secondary structure of a pleated sheet can and usually is made from a single amino acid chain. https://d1yboe6750e2cu.cloudfront.net/i/876db44ecaf5510a0c2438178140fcee11f39634

Chain yes. But a beta-pleated sheet has polypeptide chains connected "head" (carboxyl) to tail in alternating directions according to the definition of Secondary Structure in my textbook. That being the case, the head-to-tail binding can only be hydrogen bonding - much like the pairs of strands (molecules) of DNA in a helix.  And if molecules only contain covalent or ionic bonds, then the beta-pleated sheet may be one chain but it is multiple molecules.

no look at the image I linked it is a single chain, covalent bonds all the way through, that folds back on itself forming additional hydrogen bonds. DNA is the wrong analogy RNA which can fold back on itself and link is a better comparison. Here is another even better illustration. https://upload.wikimedia.org/wikipedia/commons/thumb/1/10/Alpha_beta_structure_%281%29.png/270px-Alpha_beta_structure_%281%29.png

Thank you for staying with me on this one, John. The link you provided was of a very small picture and I was unable to make out the detail. So I searched wikipedia and came up with this: https://en.wikipedia.org/wiki/File:1gwe_antipar_betaSheet_both.png
It shows that the tails and heads of the amino acid molecules are attached to each other by hydrogen bonds.

Let us continue this discussion in chat.

This sort of question is easily answered by consulting and carefully reading an introductory biochemistry text, like this section of Berg et al. on line. However, as the diagrams of β-sheets can be confusing, I will summarize.

The amino acids linked by covalent peptide bonds produce a protein molecule in the form of a single polypeptide chain.
This polypeptide chain folds into a specific shape in three-dimensional space, its conformation being maintained by weak non-covalent interactions — ionic bonds, hydrogen bonds and Van der Walls interactions. (Often referred to as protein tertiary structure.) Proteins that have a roughly spheroidal shape (rather than being long and extended) are referred to as globular proteins.
Often the three-dimensional structure has large regular components (often referred to as secondary structure) because of the potential for repeated hydrogen bonding between the CO and NH of the repeating peptide bonds.

Molecular diagrams to illustrate the type of secondary structure known as the β-sheet generally show just a section of the polypeptide chain for clarity, as in the left-hand illustration from Berg et al., below:

This may give the impression that two separate chains are involved†, but cartoon representations such as the one on the right (also from the same section of Berg et al.) show that for globular proteins this is not so.
In the diagram the flat blue arrows represent β-strands that are hydrogen-bonded to one another to form a twisted barrel-shaped β-sheet. The yellow ‘rope’ between the arrows represents the continuation of the chain in the non-sheet areas of the structure.
So the possibility for confusion arises primarily from the difficulty of showing the detailed pattern of hydrogen bonding in the whole of a large protein. (Although it may also arise from the fact that it is easiest to illustrate β-sheets using the diagrams of silk fibroin — historically the first to be described — in which the sheets are very regular and flat. To an extent this is misleading as the right-hand side of my diagram indicates.)
†Footnote
Fibrous proteins, such as silk, exist in which β-sheets are formed between many different chains. The identification of the individual chains can be made unequivocally, e.g. on the basis of the gene sequence, and it is clear that the higher-order structure is composed of many individual molecules. In smaller higher-order structures, e.g. tetramers of globular proteins held together by weak non-covalent interactions, the semantic question of whether a molecule can be made up of several individual chains arises. In my opinion, this question is best ignored, unless one is studying the biophysical chemistry of proteins.

Well David, as it happens, my question is a result of taking Bio 111 in college right now. Our Pearson textbook doesn't show the ends of the polypeptide chains in the illustration of secondary structures. The illustration on the left in your answer would have provided great insight but doesn't explain the fact that proteins are called "molecules" in other parts of the text. The consensus I'm receiving is that there is no clear consensus on the definition of "molecule" with respect to bonding. Everyone does agree that hydrogen bonds between water molecules do not make all of them one molecule.

My answer assumed that you were taking an introductory course which included something about proteins, and this was likely to be dealing predominantly with globular proteins. If there is any aspect of it that is unclear or which you dispute, please tell me. As regards the meaning of the word molecule in relation to proteins in general, this is another question and concerns mainly higher order structures. If this really interests you, please ask it as a separate question. However, of one thing there is no doubt: the polypeptide chain translated from a mRNA encoded by a gene, is a molecule.

@Byron1948 your question is a natural one for someone approaching protein structure after some chemistry. Has David answered your question? Do you see that the atoms in the $\beta$-pleated sheet are in fact all connected by covalent bonds (in addition to hydrogen bonds); that the molecule is just long and flexible enough that more than one type of interaction can be involved?

Thanks Dan. No, I don't think I have a clear answer yet. The illustration on the left of David's first comment show hydrogen bonds a the ends of the polypeptide chains (the dotted lines). I'm looking for a definition of molecule in terms of bonding. If the definition is "multiple atoms bonded together", then fine. Technically all water in a drop is one molecule due to hydrogen bonds. But this doesn't sound like a reasonable definition to me. What am I missing?

@Byron1948 — Your question related to text book diagrams of beta-sheets of proteins, leading to the statement: "But a beta-pleated secondary structure would have to be two or more chains (molecules) connected by hydrogen bonds. No?" My answer was "No" — the diagram (unless it stated it was silk fibroin) represented hydrogen bonds between parts of a single polypeptide chain (and not at the ends, as you state). If you want to discuss the meaning of the term "molecule" start with Chemistry SE. Ask separately about protein molecules here when you are more familiar with different proteins.

So, dotted lines aren't hydrogen bonds then. Guess I was misinformed.

@Byron1948 — A Polypeptide chain has two ends (also referred to as termini): an amino end (with a NH3+) and a carboxyl end (with a COO–). Neither of these is portrayed in the left side of the diagram (all COs and NHs) and, indeed they are never parts of beta-sheets as they are chemically different and not part of peptide bonds. Nor, in globular proteins are they generally even near beta-sheets, as the right hand part of the diagram illustrates. And btw., although I am sure it was not intentional, the phrasing of your comment is close to violating the list's "be nice" ethos.

Thank you for the clarification. I have, as you suggested, turned to the Oxford Chemical Dictionary in order to better understand precise definitions of these terms. And, although some answers come across as pedantic and condescending, I have no intention of violating the "be nice" ethos. Most of the time I find StackExchange to be a very helpful resource.

This may be of additional help, as I used to struggle with the difference between a peptide and a protein too.
A peptide is a single, short chain of amino acids (approx. <50 amino acid length). It's a single molecule.
A protein may or may not be a single chain of amino acids. It may or may not be a single molecule, it could be several molecules adhering to each other.
Hemoglobin is a protein. It's constituents, alpha- and beta-globin, are peptides. It's correct to refer to each of them as proteins, too. Alpha-globin is definitely a protein. What you would never say, however, is that "the hemoglobin protein is composed of four proteins", two alpha-globin and two beta-globin proteins, even though it is most certainly technically correct.
If you want to be extremely pedantic, hemoglobin is a single (metallo)protein composed of four peptide molecules, which behaves as a single unit, hence why it can be colloquially but not strictly referred to as a molecule.

This is not completely right. A peptide is seen as a short chain of amino acids linked together. More complex proteins are referred to as polypeptides. Today, proteins are seen as the functional unit built from polypeptides or peptides - sometimes more than one. But a protein can also consist of a single polypeptide. What matters here is the 3D-structure.

I don't understand how this disagrees with what I wrote. It's exactly re-written. Polypeptides are multiple peptides, hence 'poly'. Proteins are either peptides or polypeptides. Peptides are arbitrarily "short" single chains. Which part is not right?

Peptides are explicitly short - not only a single chain.

I've updated my answer. 20 years ago I was taught (and older generation scientists) say that a peptide is <100 AAs long. Wikipedia states <50. I guess it's arbitrary and fashion-sensitive, but we can agree it's a "short" chain.


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Identifying a spider very similar to a brown recluse
I took this pic tonight when I saw what I thought to be a Loxosceles reclusa or brown recluse. But when I looked closer, the typical pattern on the back of its cephalothorax seems to be upside down! I tried to compare with lots of pics and I was not able to identify this one. Plus, its abdomen is kind of velvet greenish.
Could anyone help identifying this spider please? Last precision : the body size (excluding the legs) is around 1cm.
Thanks Folks!
Photo taken on June the 24th 2018 around 10pm in Toronto, South Ontario, Canada.
PS: Even if one of its leg is fully missing, it was still running very quickly...

I think this a nice male Cheiracanthium inclusum, the familiar "yellow sac spider" (outdoors edition).  The abdomen is what you would expect, the very long first pair of legs, the obvious eyes at the front of the head (middle two of the top row).
I'd feel more comfortable if I could see the usual very dark 'face' and chelicerae, but the angle of the photo is such that it might be just hidden.  The carapace pattern looks interesting, but it may well be that the flash of the photo is giving us a different look there.
Here's the link to the Bug Guide page, with a representative photo of a similar male:
https://bugguide.net/node/view/80427

source: Stack Exchange

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

sort: votes


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Isolation of Intact Granules from Mast Cells
How to isolate intact granules from mast cells without using sucrose and percoll?

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


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Electrodes in non-conducting fluid? Are they neutral? Electrolysis, Electrophoresis
I'm a moleculary biology student and have to do a detailed presentation about SDS-PAGE for my next lab.
So I was currently trying to understand the physics of electrophoresis and electrolysis. Since I was never very good at physics I wanted to make sure I understand it correctly:
Am I right in saying, that if I have two electrodes in a non-conducting fluid, that no current will flow and that thus the electrodes are not actually charged but neutral? Since if you have a normal current with a metal wire, current also does not flow, if you have a gap in the wire. The electrones are not "waiting" and the ends of the wire, if you know what I mean.
So the electrodes are uncharged, right? But if I would take salt water as the fluid, the charge can be balanced by ions, and the electrodes themselves will get charged, if we assume that no Redox reaction occurs. So that there is e.g. the cathode with an excess of electrons, and sodium ions moving towards it and then surrounding it. And the more electrons flow over time, the more sodium ions gather there. Am I picturing this correct? But since water is present, electrolysis could occur and the electrons in the cathode would get less (and more in the anode). But why can it still attract proteins and nucleic acids in electrophoresis, if the electrodes are constantly held neutral? Is it because there are constantly electrones flowing and thus the electrodes are never actually neutral?
I must say, trying to understand things in detail is very confusing, especially in physics. I hope someone can help and/or maybe recommend a book or other source where this is explained. Most books and videos only explain it superficially and jump right to equations. Thanks :))

I’m voting to close this question because it concerns electrochemistry and is therefore better suited to a chemistry or physics forum. The application of electrophoresis to the separation of biological molecules is tangential to the core of this question, which concerns the charge of the electrodes.

Electrodes are neutral, but they are held at different potential. This is similar to the current flow in a wire: although current flows, the wire remains neutral, i.e., no charge is accumulated (unless we have a capacitance somewhere in the circuit).
Analogy: flow of water
A good analogy to current flow is a flow of water in a river. The water itself is charge, while difference in height corresponds to the potential difference. It is clear that water will flow from higher ground to lower ground, but the density of water at a particular place is not changing, because, as water flows, more water is supplied from the source, while the excess water at lower ground does not stagnate, but moves further towards the sea.
Electrolysis
In electrolysis cathode supplies electrons, while the anode collects them. They are held at different potentials, so, if ions are present in the liquid, the negative ions will drift towards the anode, whereas the positive ions drift towards the cathode.
When the negative ions reach the anode, they give it their excess electrons, contributing to the current flow. The ions themselves transform in neutral molecules and condense on the anode. Similarly, when the positively charge ions reach the cathode, they take come electrons and become neutral. As long as there are ions that can come and take/give electrons from the two electrodes, the current will flow. The excess electrons are supplied and taken back by the buttery that supplies the potential difference. Buttery is akin to evaporation in the water cycle in the nature in the above analogy, which takes water from the sea and back to the river source.

Thank you for the quick reply. Just to be sure: Let's say the power source is a capacitator (so just seperated charge, which creates a potential difference). Would that mean, that if the fluid is not conducting, that no electrons flow from the capacitator to the electrode? Or wait, do electrons even "flow"? And since you said the electrode is always neutral - why are positvely or negatively charged ions attracted to them?

If the fluid is non-conducting, the current will not flow. Note however, that a capacitor is not a buttery - if a current flows, it gets discharged, i.e., the potential difference will decrease and the current would eventually stop. The gravitational potential that make a river flow is very similar (even mathematically) to the electric potential - why does water in a river flow, even though there is no empty space ahead?

Yes, that makes sense.
Can you have a current without electrolysis?


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Migration of cut vs. non-cut plasmid on gel
As you might know there are 3 common forms of a plasmid:

ccc-form (CCC), being supercoiled.
oc-form (OC), being nicked and therefore relaxed.
linearized form (L), being cut on both strands and linear.

In theory the fastest migration should be the CCC, then L and the slowest is the OC-form.
Source: https://www.sciencedirect.com/science/article/abs/pii/0147619X81900123
So I have a plasmid with 7631 bp from a Midiprep. I cut this plasmid with NotI and put both versions on a gel, to check for the quality of the Midiprep.
I expected my plasmid to have the CCC form and therefore be faster (lower) than the cut L-form.
I ran the gel and the result is the opposite. My plasmid runs slower (higher) than the cut version.
Why is that? Do I have a misunderstanding somewhere? Is my plasmid ok?

For clarification: NotI- means that the plasmid is not cut. NotI+ means that the plasmid is cut (and therefore linear).

What organism are you propagating your plasmids in? What kind of gel / buffer are you using?

E. Coli (DH5-alpha).
This is a 1% agarose gel with 1x TAE.
Digest was done with NEB enzymes and CutSmart-Buffer according to protocol. Non-cut plasmid was treated the same, but without enzyme.

What kind of plasmid prep are you using? I remember having rarely seen the ccc form. If all three where present, it was usually the weakest band.

What do you mean with plasmid "pred"? The kit is from Qiagen. The plasmid itself is a vector for lentiviral transduction. I'm just confused because only the oc-form would be slower than linear. But I don't believe that all my plasmid is nicked.

@FelixH. Pred -> prep. If you are new at this game, you probably won't see much supercoiled, mostly circular or nicked circular. Supercoiled can also run in quite a few positions depending on the state and if you overloaded or not.  I'm assuming that the NotI+ is running at the correct size (only 1 cut site)? If so, don't worry about how the uncut is running too much. That looks like 1kb plus ladder; if so, size is right.

It should have been "prep", a simple typo. Otherwise I agree with @bob1

@bob1 Thank you for the reply! I'm not particularly new at these things, but once in a while I try to ask myself questions that are considered "basic" or "easy" but most (even advanced) scientists around me do not seem to have an explanation for. A good midiprep should be mostly supercoiled. bitesizebio.com/13524/… pubmed.ncbi.nlm.nih.gov/22693686
It also does not seem to be overloaded, since its roughly 200 ng/µL (diluted midi).
The cut is the correct size and yes NotI cuts one time in my plasmid.
The ladder is 1kb+.

Just for clarification, I know that the midiprep is probably fine, but I experience so often that people around me tell me "that's just the way it is", instead of trying to find proper explanations. I'm just curious why my results do not fit with the standard theory/papers of plasmid migration.

@FelixH. always good to challenge the paradigm! I agree your midiprep looks good.  In my experience, supercoiled can run in a number of positions relative to cut; I can't recall exactly the reasons I was taught many years ago, but I think residual protein contamination, entangling of the ccc form with others, and overloading/underloading all play a role.

@bob1 Thanks for your reply. Entangling sounds like a reasonable explanation - I think I have even read that somewhere recently, when I was trying to find an answer.


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Spike protein production by mRNA vaccines?
I am trying to understand the spike protein production mechanism of the mRNA vaccines, and during my research I learned that the mRNA (Moderna, mRNA-1273) vaccines hijack the cell machinery to produce spike proteins of SARS-CoV-2 by providing genetic material mRNA (which is encapsulated by lipid nanoparticle).
My question, which cells are subject to the vaccine particules (which factor determines the target cells?) Are produced spike proteins part of the cells (which interacted by the vaccine), or are these proteins emitted into the bloodstream like hormones so immune systems attack only the produced spike proteins?
I am asking this question to understand whether the cells which are used to create spike proteins are attacked by the immune system.

I am asking this question to understand whether the cells which are
used to create spike proteins are attacked by the immune system.

Yes, that is the aim of RNA vaccinations!
But don't worry, that's a good thing, as can be concluded from this review-paper, that emphasizes the advantage of RNA vaccinations to invoke cellular immune response:

Although subunit vaccines have been used successfully to elicit
humoral immunity against a wide variety of pathogens, they fail to
induce cellular immunity which is required to eradicate the
intracellular pathogen reservoir of many chronic diseases, including
viral infections such as HIV or hepatitis C.

Basically, the idea is that presented antigens from traditional vaccines are inclined to be presented via MHC2, rather causing humoral immunity, while after RNA transfection, cellularly produced peptides can also be presented on MHC1, causing cellular immunity.


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Sequence between PolyA signal and PolyA tail
Between the polyadenylation (PolyA) signal (AAUAAA in humans) and the start of the polyA tail, there is a short sequence of about 10~20 (G/U rich) bases, is there a special term for it?

Image credit: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175714/

Does this region have any regulatory effect? When artificial mRNAs are made, the polyA tail is often just stuck to the end of the stop codon, omitting the polyA signal and this intervening sequence. The mRNA still works to produce protein, but could this sequence affect the amount of protein or duration of expression?

My guess is that the GU rich region helps to keep the pre mRNA in place before endonuclolytic cleavage occurs.

I am not aware of a particular term other than more generally referring to the sequence between the stop codon and the polyA tail as the 3'-UTR.


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How are animal patterns encoded in the dna?
After seeing the patterns on the feathers of a argusianus argus pheasant (shown below), I am curious where is the information that encodes a pattern for a particular bird, and what form is this information in?
On the bird below, there is a pattern of gradient in a circle, wavy stripes, spots, a very soft caustic or honey combed pattern, among others.
I am interested in both the process of producing this pattern in a particular bird (which proteins do what), and also what coordinates this process (what in the dna controls these proteins).
For instance, some guesses: maybe some random seed is encoded in each organism, and that determines the initial conditions of some proteins, which through a cellular automata type mechanism the patterns are randomly but reproducible produced in each feather (I think this is similar to the reaction diffusion idea). Another possibility is that the information in the pattern is encoded somehow, pixel-wise (crazy!), in the JPEG style DCT basis, in the JPEG-2000 style wavelet basis, in the gabor basis, from some deep representation of some neural network, or something else.
Any insights and links would be appreciated.


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Experimental methods to demonstrate coupling of GPCRs
How would you experimentally demonstrate receptor coupling through each of the G proteins, Gs and/or Gi?


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Are microtubules in centrioles helical, like they are when in isolation?
Microtubules tend to be of a helical structure, do microtubules in centrioles also have a helical structure?

The centriole is composed of nine circularly arranged triplet microtubules, one complete microtubule (the A-tubule) onto which two additional partial microtubules are assembled (the B- and the C-tubules, respectively. )
What are the structures of A, B and C respectively, are they helical?

As far as I'm aware, microtubules that are composed of the same constituents will always be structurally identical. This will probably help you:
https://en.wikipedia.org/wiki/Centriole There's a couple of nice diagrams

plenty of diversity,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5662251/


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Does evolution produce organisms perfectly adapted to their environment?
I have this biology assignment with this chosen topic. I have no idea where to start researching. I have studied the mechanisms and theories of evolution. I just don't know which relates to the topic. The task is to persuade an audience of one side, either yes evolution produces perfectly adapted organisms or no evolution does not produce perfectly adapted organisms. I have started research on the blind spot of the vertebrate eye and that might be case scenario for the topic. If you have anything to add at all that would help me complete this project. It is much appreciated. Thank you in advance!

Hello and welcome to Biology.SE! Take the tour to learn about this site and earn yourself your first badge.

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

Perhaps an angle which hasn't been covered yet, which can be used as an argument against the vague question "does evolution produce adaptations to better suit an organism's environment":
Sexual selection contributes to the acquisition of traits which are favorable in mate choice or competition for mating. For instance, ornaments such as antlers are considered attractive for others in the species (female mate choice); they also aid in male-male competition (resource-defense or female-defense mating systems)
Here is an excerpt from an essay I wrote many years ago:

Sexual selection in particular has the peculiar tendency to exaggerate
  traits even beyond their ecological optimums. [...] Megaloceros giganteus, the Irish elk, is an extreme example of
  a recently extinct animal (estimated to have disappeared 10,600BP)
  whose antlers and body size were grossly unfit for the increasingly
  distressing requirements of its woodland habitat. It stood at 210cm at
  the shoulders and its antlers spanned a width up to 365cm, weighing as
  much as 40kg. It is conjectured that extinction came as a result
  of the inability to further sustain the exaggerated trait, which
  required calcium and phosphorus replenishment as well as repletion of
  fat reserves from a rapidly shrinking high-quality forage density as a
  result of climate and eventual environmental change.

Of course, there are hundreds of examples of this. I just like the Irish elk. It was imposing, to say the least.

I must also stress that your original question betrays ignorance on the topic. Evolution is not teleological, it has no end goal. Also, very crucially, the environment is ever-changing - abiotic factors such as temperature, as well as various pressures from other cohabitants in the ecosystem, are always changing. Perfection implies an end, stable state. A 'perfectly' healthy, immune individuals will eventually become vulnerable to a pathogen or parasite. Perfection is also subjective, and means nothing in biology. In photosynthesis, the theoretical maximum efficiency of solar energy conversion is approximately 11%. Yet plants are ubiquitous. Birds have light, hollow bones to aid in flight; the eyes of eagles are better suited for visual feats not shared by humans; cats have great night vision; bats have an expanded range of hearing due to their use of echolocation; insects have well-developed and highly sensitive olfactory systems, etc. None are perfect, and can always be improved upon, theoretically speaking. And what use is night vision if there is no night? What use are exceptionally light bones if you are a flightless bird such as an ostrich?
My answer to your question is this: evolution never produces perfect adaptations, it may only sometimes produce traits which, to humans, are impressively advantageous. Biology is full of imperfections; evolution can only work with pre-existing structures so it does not explore all possible solutions, where you could likely find something resembling perfection. Evolution produces organisms with traits which are or once may have been capable of allowing the organism to survive. Nothing more.

You should most definitely have a look at a very introductory course to evolutionary biology such as evo101 for example.

Does evolution produce organisms perfectly adapted to their environment?

There is a lot to say about this question. The question is very broad and cannot be fully answered in a single post. The very very short answer is "no". I will very briefly develop this "no" below.
Concept of perfection
There are semantic (and hence philosophical) issues of the concept of perfection in this question but I shall not go into these issues. Typically, in the fact of sexual selection (and other arms race), the concept of "perfection" becomes very unclear (see S Pr's answer).
There is variation in populations
Evolution is all about genetic variance in populations. The fact that variance exists makes that necessarily there is no notion of perfectly adapted for a population (or for a species) as not all individuals are the same!
"Drivers" of evolution
Evolution is a change in allele frequency over time. There are a number of drivers of such changes, including natural selection, genetic drift and mutations.
While natural selection is a deterministic process, genetic drift and mutations aren't. There is hence constantly departure from a "hypothetical perfect" caused by genetic drift and mutations.
Mutations, while being a "random process" (see Are mutations random?), most mutations are deleterious, hence constantly inputting "imperfection" into populations.

Hi Remi. I see what you're doing ;) You're stiff competition, friend!

Sorry, I failed to refer to your answer. Obviously, I added a note inspired by your answer and I should have linked to your answer. Done, now! That being said.... Wow you've been fast at detecting it!

No problem, just joshing. I wanted to say hi because I see your answers quite frequently and I'm more-or-less a new person here. Hello!

Another factor here is that natural selection pressure is asymptotic.  Even if we could provide a constant environment, and define what is perfect adaptation to it, the closer individuals get to that perfect adaptation, the less pressure there is to improve.  Reaching perfection would take infinite time, so evolution generally settles for "good enough".

@jamesqf Interesting point. While it is true that selection pressure decreases with decreases additive genetic variance and hence with increased allele frequency (past a certain frequency threshold that depends upon the dominance coefficients), a statement like "the more fit an individual is, the less likely it is for a new mutation to be very beneficial" would be true depending upon the mutational effect model considered. It is standard to use a geometric model and empirical estimates appear to be quite supportive of this model.


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Do different microscopes and attached cameras differ in crop factor between each other?
I analyzed a bunch of microphotographs recently and used "% of image area" to describe the area of structures (chorionic villi, had to show their density in placenta). However my professor suggested I should have used mm2. There is no problem in conversion, but I suspect different microscopes may have different areas of field of view for the same scale. Thus the conversion will make the results just more difficult to interpret.
So does the absolute area of microphotographs of the same scale and size differ between microscopes/cameras? Or is it somehow standartized?

Thus the conversion will make the results just more difficult to interpret.

I'm not personally familiar with this specific measurement, but in general, unless there is a specific convention in how to report a measurement, an absolute measurement should make the results easier to interpret, not more difficult (vs. % of image area). From a quick search, it seems like absolute measures of area, volume, and density are typically used when reporting chorionic villi measurements, so there isn't a convention to do it another way.


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Branch length in phylogenetic trees
I know this is a very basic question, but it is not too clear to me what is the unit of measure of branch length in phylogenetic trees.
I have come to understand that it is usually expressed in number of substitutions/site/some unit of time.
What is that "some unit of time"? Generations?
Does it depend on what method of tree construction I am using (NJT, MP, ML)?
Thank you for your time.

It does depend greatly on the format, in some diagrams it is meaningless and just created by what is necessary to make the tree visibly clean. Make sure the diagram intends for it to mean something first.

@BeatriceBaldi See the chat for ongoing discussion.

When you estimate a phylogenetic tree, be it by likelihood, parsimony, or distance (like NJ), the lengths will be given in units of substitutions per site, with no time information. For example from here:

The units of branch length are usually nucleotide substitutions per
  site – that is the number of changes or 'substitutions' divided by the
  length of the sequence (although they may be given as % change, i.e.,
  the number of changes per 100 nucleotide sites).

To transform these lengths into a time scale, further information is necessary. For example assuming that the molecular clock is valid, or instead using relaxed clock models that describe how each branch length l=r x t can be decomposed into a rate r and a time t. Since in many cases the rate is not constant along the tree (i.e. the clock is not valid), an inferred phylogenetic tree is not ultrametric (i.e. the sum of branch lengths from the leaves to their MRCA is not constant).
There are software packages, most notably BEAST, that explicitly model a strict or relaxed clock for you, and then can return the branch lengths in arbitrary time units. "Arbitrary" means that the numbers by themselves do not have special meaning, and will reflect your choice for instance of the prior. In which case they can represent year, million years or generations (http://beast.bio.ed.ac.uk/faq#Evolutionary_rates_and_time_scales).

I think it is important to separate the proxy used to estimate time with time itself. There's two solutions to the answer either "time" or "it depends upon the methodology used". However, in the second case one will note that whatever statistics is being used it is always a proxy for time. One will also note that many tree are being build as a congruent of various proxy so that the branch length are the best possible estimates of time. The overal goal of the tree representation is the time from lineage to their MRCA.

The branch length unit of a phylogenetic tree is always "substitutions per site" (the only info we have from sequences alone). No discussion there. Pls check the books by Felsenstein, by Ziheng Yang, the timetree resource, or the manual of any tree inference program. To interpret as time, usually you're assuming a (strict) molecular clock. In this case you are in fact claiming that the rate is constant (then branches are proportional to time). The lengths are NOT the best time estimates unless the sequences do follow a strict clock. (tests for clock-likeliness use this very fact BTW.)

How about phylogenetic trees based on phenotypic data and carbon14? Do you think it is wise to consider that there is no universal meaning to the length of a branch in a tree as it depends on the technic rather than saying that the length of the branches express some proxy for time?

I can't comment on wisdom, I am only answering the OP's question. Morphological data has the same interpretation as sequence data, and also need a model to disentangle rates and times, since the lengths describe only their product. I am happy to explain more through the chat. (By your comment on carbon14, for fossil ages, maybe you are thinking about "total evidence approach" and other dating methods? They are based on relaxed clock models.) And yes, there is a universal meaning for branch lengths -- that is my answer.

Let's continue in chat...

Thank you and @Remi.b your answers and chat were both helpful! What I was looking for was exactly what you said, that in all those methods of tree reconstruction that I mentioned (starting from sequence data), the branch lengths given are in units of substitution/site. Then of course, to have information about "absolute" time, we have to apply a molecular clock (be it strict or relaxed) and a calibration point (be it fossil data or biogeographical events). That way we can calculate time as branch length/mutation rate.
Thank you both so much, it's great to find such a helpful community!

This answer is mainly inspired by a long discussion in the chat with @LeoMartins.
Branch length represents some measurement of lineage divergence
Branch length represents some measurement of lineage divergence. The actual measurement depends upon the type of data considered. For genetic data, it is generally (if not always) a number of substitutions. In any case, those measures of lineage divergence are not a priori design to be best estimates of time, however they are often good proxy for time and often interpreted as being measurement of time.
Cases of meaningless branch length
Be careful that some trees use branches only to represent evolutionary relationships but do not convey meaning via branch lengths.
Total evidence approaches
More and more often, we make consideration of "total evidence approaches" (e.g. Arrigo et al. 2013) which can use sequence data, fossil data and morpho data to form a consensus and offer best estimate of lineage divergence.

The length of branch indicate time in years (or whatever standard objective unit of time). It would make little sense (although one could argue that it'd be interesting to look at) to build a tree of life where time is in generation as the generation time varies so greatly among lineages.
It is important to not confuse the mean of estimating the length of a branch to the length of the branch itself. For this I will just give you two technics used to estimate such branch length.
Number of substitutions
Now, we estimate this time based on a number of method. One of them is the number of substitution at neutral sites. The number of substitution at neutral sites over $n$ generations is equal to the mutation rate $\mu \cdot t$. That's a classic result, it is due to the fact the there are $2 N \mu$ mutations at each generation, each of them having probability $\frac{1}{2N}$ to fix (given they are neutral) and therefore the neutral substitution rate is $\frac{2N\mu}{2N}=\mu$.
So, using substitution rate we can estimate the number of generations and by estimating the generation time, we can estimate real time (in years).
Most of the time the length of the branches are simply the number of observed substitutions but as not all phylogenetic trees are made from such data, one must consider the branch length in phylogenetic trees in general as being measure of time.
Fossil data
Other methods exist to estimate the length of branches such as fossil datation for example. Here we directly estimate the time in years, not in generation first.
It is important not to confound the mean of estimation of time with

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Dissolving cell pellet after sonication
I was doing a protein prep and I made a mistake. After sonicating my cells, I was supposed to centrifuge and collect the supernatant (my protein is soluble and comes in the supernatant). I however, forgot to centrifuge and loaded the entire solution after sonication (debris and all) onto a Ni-NTA column.
Is there any way to dissolve the cell debris so that I may be able to recover the NTA beads?

Follow the instructions that came with your column for cleaning. The resin will probably be fine, but you'll need to thoroughly clean the column. My GE columns recommend washes of:

20% EtOH
30% Isopropanol
1M NaOH
1M NaCL
SDS in 0.1M Acetic Acid
Stripping buffer (EDTA)

Wash between each with several column volumes of distilled water. You may not need to do all of them. Then just recharge your column with a 100 mM Ni solution (or metal of choice)

You could try to resuspend everything and carefully decant, this would get rid of most of the cell material, as the beads will sediment much faster. Then wash the column with a ridiculous amount of acid or base.
But you should just discard everything and take new beads, they're not that expensive (maybe 10-20$/ml resin).

You might also try washing with guanidinium.

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


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Name of this plant
I contact you all with great pain because my cute little plant is slowly deterioriating. I need you help. Do any of you know the name of this plant and/or the caring specifications for it? If it helps, it stays in South America.
Thanks you all.

Do you think it is native in South Africa or do you think it could be ornemental? If it is ornemental, you will have better chance of getting an answer on Gardening.SE.


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Why is my white hair turning black/dark brown?
The only change I have made is I started taking a multivitamin daily (centrum silver, men over 50) about a month ago....Now I see black hairs in my beard and on my head.  I was prematurely gray (started at age 20) and have been completely gray/white for the last 20 or so years. Just curious...


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Does mechanical shock kill animals?
I heard that loss of blood kills shot animals, a lot. But a few times, I heard that mechanical shock kills animals. For example in this video (starts to play at the right spot; relevant from 14:35 to 15:03).
That loss of blood kills an animal seems pretty obvious as the brain can't function without being supplied oxygen and it can't be supplied oxygen if there is no blood to carry the oxygen.
If the mechanical shock is applied to the head, it also seems somewhat reasonable. I guess it could be that the shock destroys vessels in the brain. But other than for a headshot: Is there a biological reason why an animal couldn't continue to live after experiencing mechanical shock due to being hit by a small projectile (being hit by a truck which is able to accelerate the entire animal doesn't count)?

@canadianer Yeah, moving. Of course, you can move a car slow enough so it's true. If you move a car slow enough, its kin. energy is equal to that of a flying fruit fly. Example: The mass of the bullet an AK 47 fires is 7.9 g = 0.0079 kg. Its muzzle velocity is 715 m/s. A car typically has a mass of at least 1000 kg, so let's take that. The kinetic energy of that bullet is equal to the kinetic energy of the car when the car moves at sqrt(0.0079 kg * (715 m/s)^2 / (1000 kg)) = 2 m/s. You don't die when hit by a car moving at 2 m/s. Alternatively, you could walk against a car with 2 m/s.

Yeah I pressed the square root button instead of the square button in my rough calculation. I'd better just stick to biology…

With a small projectile you will always get some sort of shearing forces: the tissues directly impacted will accelerate faster than adjacent tissues, and so on. This can cause tearing of many tissues, including blood vessels, but other tissues as well.
In the context of the brain, the effects of traumatic brain injury are a constant area of research, for example see here.

But is that shock sufficient for killing a reasonably-sized (deer, wolf, human) or big (giraffe, elephant, hippo) animal? Is it what actually kills an animal when a hunter shot it? As stated in the question, the effects of hitting the heat aren't in particular interest for this. Typically, less fragile parts of an animal's body are hit. You probably could die if someone threw a rock at you hard enough and hit your head but you wouldn't die if that rock hit your stomach or thigh.

Usually hunters are aiming for vulnerable organs like the heart. If a hunter hits a deer in the gut, it will probably die later from blood loss or much later from infection. If your side-view mirror clips a deer in the head as you drive by, you might cause enough concussive force to cause death even without vascular trauma, though both would be a factor.

But if the hunter doesn't hit a vital part (e.g. hits the deer's thigh), can the shock kill a deer or will it just really ruin its day and handicap it?

I can't think of any reason, besides the possibility for blood loss, eventual infection, or a secondary cause due to impaired mobility, that a gunshot to a deer's thigh would kill it.


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ID request ~2mm insect monstrosity
This tiny monstrosity (~2mm in length) was inside of some kind of "flat tent cocoon" on a pepper plant leaf in Washington state, USA.
Not sure what's going on here. Is it malformed or infected?

Could you please attach an image of the "cocoon", it should be helpful

@Algae I don't have the image, and now the "cocoon" is destroyed. It looked like a flat round bit of insect silk on the leaf, the insect was in the center under the silk, thus giving it slightly "tent" appearance.

@SergiiDymchenko did the cocoon look like this or like this?

Also, is that "fluffy" lookign stuff in the rear of the insect simply rolled-up "cocoon" or did it appear to be coming out of the insect's abdomen? Could you describe its texture?

@theforestecologist the cocoon looked more like the first example you posted.
The fluffy stuff looked like it was growing from the abdomen, it was rigid and looked a bit like fungus (but probably not fungus). I was suggested elsewhere that this is a failed to develop micromoth pupa, and the stuff is hairy larval skin.

pretty sure its of the hyperorder Hymenopterida, probably Apoidea possibly lepidoptera

It looks like Lepidoptera to me. It did not properly eclose from the cocoon and the wings did not unfold properly before hardening, which is the reason for the odd appearance, but I'm pretty sure I can see some of the anterior wing veins branching in the section facing us.


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ID request - small green caterpillar
This was eating my mustard spinach (Brassica rapa subsp. nipposinica) plant in Washington state, USA; about 1cm in length.

That's a really beautiful photo! Can I ask how you got it on such a pure white background and yet the hairs show up so nicely?

@uhoh Thanks! I spent quite a lot of time editing the image: used various masks to select non-green and almost white things and make them white.

I don’t know the exact species but he is a type of inchworm.

I was going to say Pieris (cabbage white), but those aren't "inchworms".

I went to images.bing.com and typed Brassica pest lepidoptera, which led immediately to photos of the cabbage looper (Trichoplusia ni)
I thought this image was particularly persuasive.

Nicely done, I don't know how I missed it.


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Why are there 10 base pair steps, not 16?
In a biochemistry course I'm taking, the lecturer emphasised that there are 10 possible base pair steps; I've included a screenshot of a slide stating this. This confuses me, because I cannot work out why it's not 16; why are the 6 greyed out in the image not allowed (for example, CG stacked on CG counts, but GC stacked on GC doesn't)? TA|AT is listed as distinct from AT|TA, so it's not that the greyed ones are redundant.
I've found a couple of papers mentioning that there are 10 base steps, but not why. (I can't get hold of the lecturer.)
Thanks in advance!

CG stacked on CG and GC stacked on GC are the same step with the chain turned by $180^\circ$, so there is no need to count it (and other similar steps) twice.

@Vadim, would you mind expanding your comment as an answer?

Unlike RNA, where the sense of the molecule is unique, DNA is double stranded, with the two strands having the opposite sense. In the sense of chemical stability it odesn't matter, which sense is considered positive, and which is negative.
Thus, if we consider a base pair step WX|YZ, we have Y folowing W on the positive sense strand (W->Y), and X following Z in the negative sense (antisense) strand (Z -> X). This means that, if we labeled the strands differently, we would have Z->X on the positive strand and W->Y on the negative one, i.e., we would have base pair step ZY|XW. I.e., the general symmetry rule is
$$
WX|YZ \rightarrow ZY|XW
$$
In particular, this means that CG|CG is identical with GC|GC, whereas TA|AT is identical with itself, rather than with AT|TA.
Visually, this symmetries are obtained by rotating the image of the base pair step by 180 degrees, as can be readily seen in the image provided in the question.

Maybe worth pointing out that OPs own image demonstrates why there is 10. It shows the 16 'possibilities' and grays out those that are duplicate via rotation. With the picture in hand you can just... count.


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gene mutation occurs on two strands of DNA or just one strand?
Suppose we have one strand with 3'-AAA-5' and the other strand is 5'-TTT-3'.
So when point mutation occurs, does it happen to two strands at the same time? e.g. 3'-AAA-5' becomes 3'-AGA-5' and 5'-TTT-3' becomes 5'-TCT-3'?
Or the mutation can occur with only one strand? e.g. only 3'-AAA-5' becomes 3'-AGA-5'? but in this case, A would pair up with G.
When transcription starts, the 3'-5' strand is transcribed, if the mutation does no occur in this strand, does it mean this mutation wouldn't affect any downstream products?
Is it same for indel?

A "mutation" is a permanent alteration of the genetic composition of an individual. To obey this definition, a base change in one strand must be accompanied by a corresponding change in the opposite strand. Only in this way a mutation can be transmitted to the offspring.
The situation where only one of the strands has undergone a base change constitutes a pre-mutational DNA damage, as the double strand will show a deformation at that site. The enzymes of DNA repair mechanisms recognize and correct many such "deformations", but sometimes they do not know which was the original base, and introduce a change that become fixed in the DNA sequence.


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What is the mechanism through which fractals arise in plants and animals?
Many biological organisms -- such as trees, broccoli, and the blood vessels in animals -- can be approximately described using fractals.
What is the reason behind such fractals? Specifically, do we know of the way certain cells split that lead to fractals? Do we know if there are specific genes that tend to generate fractals?

because fractals are emergent structures created by simple rules, as are many biological structures. The same kind of simple recursive signals that lead to fractals are simple enough to be stumbled on by biological evolution and are effective ways to deal with the scaling problems created by the square cube law.
https://www.complexityexplorer.org/system/explore/model_series/pdf_files/000/000/008/original/Biological_Scaling_Series_.pdf?1554498961
https://www.jstor.org/stable/2898653?seq=1

Essentially, eukariote cells use internal and external signalling hormones, so the cells can have a front/back/top/bottom end and can orient themselves at specific angles using signalling hormones, which also travel outwards through chains of cells and form signalling hormone concentration gradients. Eventually, when the gradient reaches a certain level, it can cause a distant cells to divide in two resart the gradient, so that very precise distances can grow using very precise angles.
The research on genetics related to the dendritic morphogenisis in trees, neurons, lungs, ferns and other forms in nature, doesn't give a clear summary of the process that you thought it can.
There was a patent of a technology called "Fractogene" quoted by some serious research, and doesn't involve coherent propositions and sentences! if you can figure out what FractoGene was, please comment!
You'll find talk about P-cells, Cytoskeletons, Drosphila, Danio, meristems, concluding:
We expect that a new generation of data mining tools will be required to support recursive fractal geometrical, combinatorial, and neural network models of the genomic basis of morphogenesis.
A fractal can be written in 3 instructions (copy, advance, divide) so the cells only have to have 3 behaviours to create a fractal, it's very simple. Even H2O and NaCl can form dendrites similar to plant roots, so fractal genes have an fairly simple basis.
Dendritic gold:

dendritic copper:

dendritic manganese oxides on limestone:

Even pure water forms branches similar to trees. Something so simple to generate in nature is likely to have parallel evolution of many thousands or millions of genes that regulate the precise shapes of the fractals in many organisms.
What kinds of signalling hormone gradients and genes regulate branch and leaf vein angles are very obscure and I didn't find much about "branch angle gene regulation".
You'll find information like: "The plant hormones cytokinin, auxin and gibberellin are crucial during root development." cool description of plant hormones
Here's the best read I found on the subject:
https://dev.biologists.org/content/147/10/dev184499
The most confusing to read:
https://pubmed.ncbi.nlm.nih.gov/16527761/
I scanned through 15 research papers and very few claim to have found the mechanisms that regulate the morphogenesis of fractals in the natural world.

Firstly, it is necessary to note that fractals are not unique to live things: for example, a seashore is an example of fractal structure (with theoretically infinite length).
In regard to trees and broccoli, it is necessary to note that fractal structure maximizes the area, given the same volume, as opposed to other shapes (e.g., a spherical organism would have most of its cells inside the sphere), thus increasing the area exposed to sun and facilitating photosynthesis. As such, having such a shape increases the fitness of the organism, and almost certainly is encoded genetically as the result of natural selection. For example, see here.
Let me also bring the attention to the fact that fractals occur also on single-cell levels, such as the dendrites of a neuron.
Update
Fractals are more ubiquitous in live nature than it may seem at the first glance. The obvious examples are the shapes of trees, vascular systems (of trees and animals), neural networks, etc. Less obvious examples (because of being somewhat abstract) are metabolic networks, community food network patterns, and possibly ecen evolutionary patterns (depending on whether we believe that evolution has explored all the possibilities).
West an co-workers have used fractals to explain the scaling laws relating many biological quantities, e.g., such as basal metabolic rate and the lass or organism
$$
Y=Y_0M^{b}, b=\frac{3}{4}
$$
See here for general review and the references, but also the references by @John in the other answer. While purely geometric arguments would imply scaling laws proportional to $b\propto 1/3$ (since volume scales as length to the thirs power), the fractal nature of these networks allows to infer the correct exponents, $b\propto 1/4$.
The theory by West et al., is based on three assumptions:

networks are space-filling in order to service all local biologically active subunits;
the terminal units of the network are invariants;
performance of the network is maximized by minimizing the energy and other quantities required for resource distribution.

The third assumption, maximization of energy, is essentially the requirement of the maximum fitness. What appears to be somewhat fo an open question is to what extent the the living organisms evolve towards fractal structures or whether it is characteristic of all the living organisms, inherited from the most recent common ancestor.

What evidence do you have that fractals increase fitness? Given that this claim is at the center of the part of your post that actually answers the question, you need to provide support for this claim. Many plants, by the way, receive much more sun than they can use and therefore would not see any increase in fitness as you posit

@theforestecologist I have expanded this answer.


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What is the function of Xylem parenchyma?
why xylem need parenchyma cells ihave read these cells are connected with xylem by plasmodesma i know that plasmodesma is to connect between cytoplasm of two cells and xylem is dead so what is the need of xylem parenchyma ?

I would like to aswer your question. First definition, function is from this web:

The xylem parenchyma is comprised of parenchyma cells. Parenchyma cells are the only living cells in the xylem. They have thin cell walls, large vacuoles, prominent nucleus, and protoplasts. They have differing shapes although they are usually cylindrical and lobed in form. In the trunks of woody plants, the xylem parenchyma cells are colourless and are believed to be involved chiefly in storing starch, oils, and other ergastic substances. The inclusions in xylem parenchyma cells may contain tanninferous compounds.

And from this article:

Xylem parenchyma cells in contact with xylem conduits are assumed to simultaneously generate the energy gradient (deposition of solutes in the form of sugars, ions or a combination of both) that allows water to flow into empty vessels/tracheids, and supply water for refilling (Zwieniecki & Holbrook, 2009). Regarding the first task, the initial research focus has been on finding the source of osmoticum through analysis of carbohydrates in the parenchyma cells and the role of phloem in the delivery of sugars to sustain refilling. Both enzymatic analysis and visualization techniques have demonstrated that starch levels in living parenchyma cells adjacent to xylem vessels decrease on a timescale coincident with embolism refilling (Bucci et al., 2003, Nardini et al., 2011a, Sakr et al., 2003, Salleo et al., 2009, Secchi & Zwieniecki, 2011).


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Searching a fructose degrading bacteria
my question is do you know a fructose degrading bacteria?

Wich is straitforward to use and cultivate?

Wich shouldn't create excrements, that can't be removed simple.

Welcome to SE Biology. As a new contributor we do not wish to discourage you, but your question falls somewhat short of what is expected here. You would benefit from reading the help on how to ask questions where you will see that good questions are of general interest, provide detail and context, and show evidence that that poster has done research of his own before asking. Do some internet searching and then modify your question to tell us what you have found about fructose degrading bacteria and what you still need to know.


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Crispr complex in human cells?
Is the crispr (where the parts of Virus DNA is saved) section of the DNA existing in human cells aswell or is it just in bacteria cells?

No analogues of the CRISPR-Cas system have been found in any eukaryotic species, including humans. So far, it appears to have evolved only in prokaryotes and archaea.
Reference: Evolution of RNA- and DNA-guided antivirus defense systems in prokaryotes and eukaryotes: common ancestry vs convergence


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How loud a sound would need to be to wake someone up?
I have been researching about this and it looks like the term would be auditory arousal threshold. Imagine you fall asleep while listening to music with earbuds. Out of a sudden, the device starts playing really loud music (let´s say 40 dB higher compared to what you were listening). This sound would be quite loud that it would damage your ears.
My question is, is there any study showing which would be the minimum dB level of a sound that would make you wake up (and, well, remove the earbuds)?
I would assume this would depend on the frequency of the signals as well. But, what about the age of the person?

I don't think this is generally answerable with a single value for all people. The answer would vary from "not very loud" for light sleepers to "impossibly loud" for those who are completely deaf.

Yes, I understand what you mean. But I was expecting something like an offset that would be a general norm for most people. Let´s say: Subject A has no hearing loss and we could say they would wake with a 90 dB sound. Subject B has a hearing loss of 20 dB and therefore they would need 110 dB to wake up in the majority of cases. Let´s assume hearing loss is flat and the sound is white noise for simplicity. I have also read that the brain can adapt as well and if they are accustomed to white noise during the day, it might not wake them up.

Can we say no more damage can be caused to the ear when the threshold is exceeded an damage has been already caused? Let´s say a person with no hearing loss, according to OSHA, would not get their ears damaged if they do not listen to 90 dBA for more than 8 hours. If this limit has already been exceeded and the subject has hearing loss, can we say instead of 90 dB, they can be exposed to 90 dB + Offset for 8 hours now?

No general answer would make sense, as kmm points out. It's too dependent on the conditions and the individual: it will even vary for an individual from day to day. This is one reason alarms often have volume controls... Loud noise is not safe for people simply because they have hearing loss, if anything it's putting them more at risk for more profound hearing loss.

Ok, not even something similar to what I suggest in my first comment? I have been researching but could not find anything like this and wanted to give it a last try here. My background is EE and not medical... I can understand that someone that is completely deaf would not detect air pressure change as their hair cells could be nonexistent or maybe the nerves may be ruined. But, what if the brain gets a volume change (after the signal gets into the brain) of 20 dB, would this be enough for it to wake up?

It's not just about hearing loss. Your threshold for wake up is going to depend on how tired you are, the nature of the sound, what stage of sleep you are in, other personal differences, etc etc. From an engineering perspective, you need to consider the risks of failure: you will want a different level of sound if wake-up is very necessary (i.e., fire alarm) versus if it's okay to miss some % of the time.

@Bryan Krause: Yes.  I can be woken up by stealthy movements in my supposed-to-be-empty house, yet in my younger days slept through any number of raucous parties in neighboring apartments.

@BryanKrause, Yes, I am actually trying to look for a dB level which would guarantee that any person would wake up to (except deaf people, for sure). Imaging you have BT earbuds that play an alarm that the rate of failure must be 0%. The question would be how loud the sound needs to be and of course the type of sound. In other words, how high that threshold could reach considering all the circumstances known

@the_moon Yeah, sorry I don't feel like that's something answerable here, it's not relevant to biology, just your engineering project.

Well, it is the biology of the human ears and the auditory system. I thought that my question would be useful and interesting here. Of course, it has value to me now but it might have value to others as well.

Humans are not standardized components, which is what makes human factors engineering so hard. 80 percent of children between the ages of 2 and 13 did not wake up from a standard issue alarm.

A conventional wisdom is that a sleeping mother can hear her child crying on the other end of the house, but not a cannon firing next to her ;) So it is not just sound intensity that matters.


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What's the decomposition rate of a mammal at -20 Celsius?
Is there any where to predict it without thawing? In terms of measuring it.
What if the body was immersed in sugar prior to freezing?

What do you mean by decomposition rate, if you mean rot then the answer is none, if you are talking about other effects that would fall under taphonomy and it will be extremely slow.

Cell apoptosis.

Zero, apoptosis is programmed cell death, it does not occur in frozen tissue, do you necrosis?

Does necrosis happen then?

At -20,chemical reactions and biological activity of microbes is nearly static. The mammal can get dehydrated if the ambient humidity is low, they freeze dry animals in cold temperature, If the animal is protected from humidity fluctuations, the DNA can last 100,000 years. They just revived nematodes found frozen in ice for 40,000 years, they are multicellular.

@com.prehensible Thanks for the answer but this should not be right, i ve spoken with a specialist and was told that cell still undergo apoptosis because they are starved to death. The cells that survived being frozen.

Take a look at the frozen carcasses of mammoths and dire wolves found in the permafrost regions of Siberia... Freezer burn happens quite frequently... the outer layers of soft tissue will start drying out.
Some even say that mammoth meat was eaten at a conference in 1951
If this is true or not... A mammal carcass preserved at -20 degrees can last long... very long.
I recently thawed a crocodile, which was frozen at -20 degrees since 1986... Except some freezer burn and shrinkage of the meat within the hard and partly ossified skin, you wouldn't even think that it was frozen for such a long time.
Adding sugar decreases the freezing temperature of water and the freezing process will take longer. Given the fact, that you have -20 degrees during this step, too - nothing will happen with the carcass.
So: no rotting, no necrosis, but: long time freezer burn

Thanks for the answer but this should not be right, i ve spoken with a specialist and was told that cell still undergo apoptosis because they are starved to death. The cells that survived being frozen.

Apoptosis is not decomposition. you said Decomposition rate. the answer is - virtually no decomposition. If you want to ask about apoptosis of the cells at -20, write a new question. The cells wouldn't undergo apoptosis because they starve. they don't consume any energy at -20 so they don't respire and starve. if they cells survive they don't decompose.

com.prehensible is absolutely right. Apoptosis is not decomposition. You asked about decomposition - I answered the question about decomposition. Please tell me where my answer is incorrect regarding your question about decomposition of a body at - 20 degrees

@JulPal For some reason I don't get notified when I get a reply. I thought that decomposition includes apoptosis.


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Why do people make "aaagh" noises when they make an effort (e.g. trying to hit a ball hard)?
I'm referring to, for instance, grunting in tennis. It refers to how many tennis players make loud "aaagh" noises when hitting a ball. In daily life, people often also do this when trying to lift something heavy, and etc. Recently, I noticed cats also make a similar noise (albeit smaller) when they are jumping onto a level that they can only barely reach.
Thus, the question: are there biological reasons why people cannot help but make such noises when trying to do something physically challenging? Does making noises help them achieve it for physiological reasons, or only for psychological reasons?
I searched online and wasn't able to find an answer.

There's smattering of research papers published on the topic of grunting and physical exertion, including at least one on tennis. The ones I've skimmed seemed to have small sample sizes and focused on testing physical performance with and without grunting, not on the physiology of the act. Next time you do any kind of brief physical exertion, pay attention to what your body does naturally. Most people will inhale in preparation, briefly hold their breath at the moment exertion, and exhale through the motion. A sequence that seems to prime the body to grunt.

@MikeyC do you mind sharing the references you found? Thanks!

@MikeyC that breathing motion is called the Valsalva manoeuvre

@bob1 - The question is why do people grunt [when doing the Valsalva maneuver], not "What is it called when people take a deep breath, close their glottis and exhale against the closed glottis?"

This is not an opinion-based question; there is an answer (or are answers). I VTC because of lack of any research.

Mainly because they are English speakers - this kind of utterances is specific to a phonetic system and culture. E.g., Russians are more likely to use "ehhh/uhhh" when mzking an effort and "aye/oye" when simething hurts them (rather than "auch").

Hilarious. Agree with MikeyC and RogerVadim. Clearly the answer is so obvious, I don't think it requires a "real research answer", that's just woeful pedantry. It's not biology, just a consequence of physics. The answer to the question "why noise" is because noise/vocalization/phonation comes about when the glottis is partially closed. After closing it (Valsalva maneuver), air remains unexhaled, so remaining pressurized air follows with a vocalization as the glottis goes to a full relaxation state. Partial Valsalva maneuvers are also vocalized. A slackening glottis is the entire explanation.

@SPr - That is absolutely not "the entire explanation." Muscles groups are strengthened or not depending on if there is a grunt or no grunt (according to studies). It is indeed physiology, and physiology is part of Biology. So it is an unconscious attempt to strengthen oneself against a task. Maybe you should question your assumptions before declaring something "the entire explanation."

@anongoodnurse - I am aware of that. It was a hint to the OP of something they could research.

Thank you all. Why don’t some of you write a formal answer though?

@JLi Answer to your Q is strictly two-fold in my view: (i) people hold breaths to maximize output from muscles and afford higher rigidity, which is handy when you need leverage and power, by essentially increasing the pressure inside the torso; and (ii) people make the grunting noise because of the physics of vocalization, due to the relaxing of the glottis which must occur between holding breath and releasing breath to continue respiration. I think the semantic pedants should provide more than complaints to demonstrate that other factors are at play. Sometimes you have to provoke an answer ;)

@SPr Thanks, makes sense!


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Why does the formula for blood velocity hold true?
v = Q/A
where
v = velocity (cm/s)
Q = blood flow (ml/s)
A = cross sectional area (cm2)
So the greater the cros sectional area, the lower the velocity, assuming that the cardiac output is a constant for a individual.
But i dont understand the formula content wise, why do you get the velocity by dividing Q by A? I do understand that the units are correct, and you get cm/s as final unit.
Can anyone explain this, perhaps graphically?

In the capillaries the A must be extremely low, yet why is the velocity so small? My book says that you have to add all capillaries up, but you cant do that, since you would get the velocity of an extremely big pipe, which isnt that of a capillary?
Thanks in advance for answering.

Very relevant link https://journals.physiology.org/doi/full/10.1152/advances.2001.25.1.44

In the capillaries the A must be extremely low

For a single capillary yes, the area is small.
However, these statements are not referring to a single capillary! They are referring to the entire capillary bed when it says "the capillaries". There are many many many capillaries and their total cross-sectional area is large compared to other vessels. Blood doesn't flow through each capillary in series, it's flowing through them all in parallel.

So if it flows parallel then the Q gets divided into many capillaries, making the nominator in the formula extremely low, and the area  in the denominator as well since it is a capillary. So the velocity decreases, since Q decreases more than A decreases for each capillary.

Is this true?  c

@excellence Yes, that's true, but I think the best way to think about it is to just think of the "A" as the area for all the capillaries (so, A = N * a, where N is the number of capillaries and a is the area of one capillary). The total A is larger for the capillary bed than it is for, say, the arterioles (this is what your figure shows in the blue line). It doesn't matter what N or a is to determine velocity, just N*a.

So the book is just avoiding to explain in mathemathically, which causes confusion and i had to spend lots of time finding out what was going on

@excellence No I think they're explaining it just fine, you just need to notice that the Y-axis on the right is total cross-sectional area, not for a single capillary. If you missed that point I can see how it would be confusing, though.

Well in reality the capillaries are not bundled together an can NOT be seen as just one big blood vessel, but rather a lot of minuscule capillaries with an extremely small Area. What I mean is, how can you say the blood speed is very low there, because of a huge Area. As i said: the velocity decreases, since Q decreases more than A decreases for each capillary. Why didnt they just show it like this, after all, A doesnt increase but LITERALLY decreases, and Q does too, but much faster. The result is a low velocity. AM i right?

@excellence No, you are not right. "A" here is the total cross sectional area. That's what's plotted on the Y axis and is labeled as such: "Total cross-sectional area". This total area is large in the capillaries, which is why velocity is slow there. For the purpose of calculating the velocity as presented in this chart, yes you can consider it as one big blood vessel, and that's what they are doing. They are considering the entire capillary bed together, just like they are considering all the arterioles together, all the venules, all the larger veins, etc.

@excellence, In reality the capillaries are all bundled together: at one end by the arterial vessels back to the aorta, at the other by venous vessels on to the venae cavae,  A, the total area, literally increases as you move from the set of large vessels to the set of capillaries.  The total blood flow per second through the aorta is the same as the total through the capillaries, so the blood is flowing much more slowly through the capillaries because of their vastly larger total area.

thanks for clarifying everything, very helpful

The trick here is that 1 mL = 1 cm3 (or cc).  So if you divide cm3/s by cm2 the result will be in cm/s.  What that means is that the blood volume has three dimensions - if you picture the vessel as a simple "box", then it has widths in two dimensions, which define a cross-sectional area, and then the third dimension is the distance that the blood has moved past, through the vessel, in order to define the three-dimensional "box" of blood that has moved past as the blood moved that distance.
The principle should be familiar from the phrase "still waters run deep".  A stream that flows rapidly in a shallow cascade over rocks can abruptly become quite slow at a deep hole, as a great depth and breadth of water is sharing the work of moving forward.


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Is a large tumor is more likely to develop hypoxic regions?
It is known that cancerous tumors in humans can develop hypoxic regions where no blood nor oxygen arrive to some volume of its cells, creating a dead lump inside or around the tumor.
See Wikipedia - Tumor hypoxia.

Are hypoxic regions and regions without blood supply are more common in large tumors than in small tumors?
What is the likelyhood or frequency of hypoxic regions in small (< 2 cm) and large (> 4 cm) tumors?
What is the typical size of an hypoxic region within a tumor?

The article in Wikipedia is too techincal and very hard to be read and understood, and doesn't have an explicit answer to my question.

This isn't a direct answer because it's more of a model system in vitro, and wouldn't model in the in vivo microenvironment, but it's interesting to look at Table 1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4764677/

The prescence of hypoxia is independent of size, grade, or histology. It occurs due to a cut off in blood supply to the tumour. Or insufficient vasculature systems, meaning the oxygen cannot diffuse all the way into the tumour. Aberrant growth of tumours can increase the likelyhood of tumours developing hypoxic regions.

Hypoxic region can be formed in any tumor, big or small. But does large tumor have significantly larger hypoxic regions?

Not necessarily. Its all tumour dependant.

And statistically?

There is no relationship. The paper titled: "Detection and Characterization of Tumor Hypoxia Using pO2 Histography," looked at several tumor types none of which have a correlation between size and hypoxia.


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Why are watermelons sweeter in the center?
Today I had a slice of watermelon and when I reached the outer parts of the pulp I wondered why those are less sweet.
Whether or not the sugar occurs in crystalline form in watermelons is still an open question, but a quick search on the internet did not yield acceptably thorough answers.
The options I found are as follows (in descending order of personal preference):

Watermelons ripen from the center outwards.
If this is the case, then watermelons wouldn't grow during the ripening, right? So they would need to achieve their final size before the ripening sets in. Or maybe it's the other way around: They ripen as they grow, and as such the center has the highest concentration of sugar.
The sugar is needed by the new seedlings to grow. (Although I think this hypothesis has been disproven with apples.)

Has any of this been proven, has there been research done on this matter?

I think the cells are smaller in the center, so higher concentration of everything but water. The outside cells have a lot more space and are more watery without so much sugar, etc.


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Why are polar seas rich with nutrients and plankton?
It is well known that baleen whales migrate to the polar seas to feed on plankton and krill (marine crustaceans). The question why are the polar seas rich with krill and plankton? If the answer "it is because they are rich with nutrients" then I ask why are they rich with nutrients?

Water density and temperature is very important for understanding water ecosystems. Water is most dense a little above freezing temperature; when surface water is warmer than that, it's less dense and sits on top of cooler water. When surface water is chilled to freezing and increases in density, it can sink and mix with deeper water.
Photosynthesis can only occur in the top of the water column because light doesn't penetrate very deep. When the surface water stays warm and doesn't mix, that top layer gets depleted of nutrients. Mixing brings up anything that has settled and allows life to use the "full column" of nutrients.
See for example https://www.nature.com/scitable/knowledge/library/the-biological-productivity-of-the-ocean-section-70631438/ :

In the high latitude ocean, surface water is cold and therefore the vertical density gradient is weak, which allows for vertical mixing of water to depths much greater than the sunlit "euphotic zone" as a result, the nutrient supply is greater than the phytoplankton can consume, given the available light


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Why Laramidia is more rich in dinosaurs than Appalachia?
Most of the North American dinosaurs are known from Laramidia - the sub-continent western to the Western Interior Sea. From Appalachia, far less dinosaurs are known. However, looking at maps, Appalachia was bigger in area while Laramidia was a relatively narrow band stretching from Alaska to south Mexico.

Why there are more dinosaurs known from Laramidia and not from Appalachia?
I can think of several reasons:

Laramidia had richer dinosaur fauna indeed. Then I ask: why?
Discovery bias - West America has better sites for digging fossils: wide open badlands without obstructions such as forests and vast construction, which prevent digging.
Preservation bias - Laramidia had better conditions for preserving fossils.

I'm no expert, but I think from my readings (possibly from reading Mark Jaffe's The Gilded Dinosaur) it's #2 almost entirely.

Its not, there are just more trees over Appalachia.
its easier to find fossil in dry climates which have more exposed bedrock and sedimentary rock. We find plenty of fossils in Appalachia just mostly in mines and other large scale excavation. Any place with little to no vegetation is best.

If you want to know why arid climates are better for finding fossils, there is an existing question about that.
https://earthscience.stackexchange.com/questions/13331/why-are-many-fossils-found-in-deserts/13337#13337


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Why are monocotyledonous plants considered more evolved than dicotyledonous?
Why are the following characteristics advantageous for a plant?

to have atactostele instead of eustele
to have less stamens
to lose secondary growth
to switch to anemophily pollination (also if it's not always the case)
to use the cotyledon as storage media instead of endosperm

Why are there so much similarities between liliopsida and gymnospermae?

This wasn't an homework question, but a genuine curiosity that arose studying such organisms. I'll be glad to modify it to fit the rules of the community if possible.


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Are gametes diploid or haploid?
Some sources say that gametes are haploid, some say that they are diploid.
I'm confused.

Could you give a source that says gametes are diploid, or that zygotes are haploid? It is hard to tell what it is that's confusing you here; the answer to your question is normally an elementary Google/Wikipedia/biology textbook search away but presumably you're getting contradictory info somewhere, but if we don't know what that info is we can't help.

This is a confusing topic when it comes to polyploids. I don't believe the definition for haploid provided in the accepted answer is correct for all species.
Haploid refers to a cell or an organism that has only a single set of chromosomes - my interpretation is that it is only in a diploid organism such as a human that haploid means "half of the total number of chromosomes in a somatic cell", because diploid organisms produce haploid gametes.
A diploid human produces haploid gametes.
A hexaploid produces triploid gametes.
I think the confusion in the accepted answer is that gamete means the same as haploid (which of course is true only for diploids, such as humans). The triploid gametes are not haploid. The definition in my answer supports that, and indeed if you search, other definitions state this also e.g. "Haploid describes a cell that contains a single set of chromosomes".
I should add, to answer the question, that the gametes are diploid for a 4n tetraploid organism - when the gamete is produced 2 of these go to one gamete, and 2 to other (diploid). It may be that the source you read was referring to a tetraploid organism.

Welcome to Biology.SE. (+1) This is much better than the accepted answer, but I saw a few ways to make improvements. In particular, there were couple of statements that could cause confusion. The second of these I deleted since it wasn't necessary to  make your point — while "genome" can be used to refer to the haploid set of chromosomes, it usually means all the chromosomes.

Actually — it appears that we are both wrong and the accepted answer is OK. You can see this in the second sentence of the second link you provided where it says "The term haploid can also refer to the number of chromosomes in egg or sperm cells, which are also called gametes." This unfortunately means that haploid has two meanings that sometimes are in conflict — to be unambiguous we should use monoploid (and it seems to me, completely avoid haploid) ... Would you like to edit your post in light of this information?

It depends on the organism in question. (https://en.wikipedia.org/wiki/Polyploid#Examples)
Notice that the gametes carry half number of copies of the normal cells. As such a tetraploid organism will have diploid gametes.

Don't get confused by the number of chromosomes. Haploid refers to 1 set of chromosome, diploid refers to 2 set of chromosomes, triploid means 3 set of chromosomes. They don't represent the numbers of chromosome present on a set.
We human beings have 23 chromosomes on a single set. We are diploid organisms and thus all the cells of our body carries two set of chromosomes (thus 23*2=46). Our germ cells however are formed through meiosis cell division and thus they are haploid (23 chromosomes).
So, sperm cell carries 23 chromosome and egg carries 23 chromosome each. When they fuse, zygote is formed and as you can see, zygote carries 23+23=46 chromosomes. Zygote undergoes mitotic cell division and a complete human is formed. So, human zygote definitely is diploid.

Does it mean ONE SET means 23 chromosomes (out of 46).

Yes, one set is 23. one set chromosomes are present in the germ cells like sperm and egg

Gametes must be haploid because they will be combining with another gamete. Sexual reproduction works to increase genetic diversity by having two haploid gametes combine to form a new organism that has a different combination of genes than either of its parents. The new organism has half the chromosomes from its mother and half from its father.
Source from Chromosomes and Meiosis Interactive
For example, in order for humans to reproduce, a sperm cell must fuse with an egg cell, producing a zygote that has a unique set of genetic information. If the gametes were diploid instead of haploid, the resulting organism would have too many chromosomes. By having two haploid gametes fuse together, it is ensured that the new organism will be genetically distinct and still have the correct number of chromosomes that it needs.

Welcome to [biology.se]. It is great that you are contributing to this site by answering questions but please try to read other answers for a given question before answering so that there is no redundancy. Redundant answers are not useful. Perhaps you should add some extra information that is not covered by other answers.


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Sephadex column for alpha-amylase
I want to purify crude alpha-amylase with column chromatography. I am using a spehadex 75, But for some reason I can't find any information on how to make the slurry.
I can quickly find tons of information on how to pack and store a column, but what i really want to know is how much powder and buffer do I mix together?

The '75' of Sephadex G-75 refers to the water regain value, which is defined as the grams of water absorbed upon hydration of 1g dry powder, multiplied by 10 (see Reiland). Thus the water-regain value of Sephadex G-75 is about 7.5ml. This value refers only to the water contained
within the gel particles and not to the water trapped outside of the particles in a packed gel (Reiland). As a rule-of-thumb, the latter figure can be estimated to 50%.
So ... 1g of dry Sephadex will give about 15 ml of packed gel
From here: 1 g swells to 12-15 mL gel
Just a thought ...
Does alpha-amylase interact with Sephadex?  Maybe 'thinking' it resembles a substrate, and (reversibly) binding to it or otherwise interacting to cause effects in addition to gel-filtration ?


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Can any one help id this bug or at least tell me if it could be biting my kids
We live on the gold coast in australia. We started looking into what these bugs were after my son became covered in severe bites. Hes always reacted a little bit to bites but this was intense.  The initial bite looked somewhat like a raised welt which he has scratched at but now over a week later hes saying they are still itchy and even with bandaging and covering the areas hes still getting more bites.  I have attached a photo of the bugs that are around at the moment but also some of the bites. we get alot of mosquitos and midgies (sand flies) but hes never reacted to those bites like this. We have recently had a flood in the area so everything is still wet. Its change of season so its cooling down.  Any help would be amazing in helping treat our son but also hopefully prevent further issues

Questions seeking medical advice are not allowed here. You should rewrite your question so that it just about identifying the insect.

it looks like a biting midge to me.

It is certainly a Diptera. How big is it? Biting midges are usually very small, 1-3mm, this one looks bigger.


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Symmetry in Biology
It seems a curious fact to me that all organisms I can think of exhibit some definite symmetry on a large scale (much larger than molecules), and in particular mirror symmetry. Since it is so wide spread, I imagine there is some deep reason for it. One thing that comes to mind, is that it might take less genome to encode. Are there any such reasons?

Welcome to SE.biology! It's expected that you show some evidence that you've tried to research the question before posting here. Please take a read of the help centre section on how to ask a good question and consider editing your post. There is a whole wikipedia page dedicated to the topic which should be read before posting questions. Thanks.

please provide with some evidence that back you research


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What kind of spider is it and was this web built beforehand? (Surprise find)
I am surprise to find an insect caught at the end of what seems to be very long nearly invisible thread/web, most importantly where the insect is caught is actually a passage way where we enter the house so there seems to be no chance for this web to be there unless it was built in few hours!
Questions: What kind of spider could this be and could the web have been there all along or it was built instantly? Do these spiders build lots of long thread like webs in hope of capturing prey one day as I have never seen such web anywhere in my house. Will the spider roll up its prey or will eat it there? I want to know this because I am anticipating guests tonight so cant have it lingering there, unless it eats up the prey fast or takes it up to the ceiling.

P.S. I am going to let the spider do its business to see if its going to take the insect back up or will eat it there itself.

For ID questions like this, you should give as many details as you can: where in the world the picture was taken, what time of day, etc. and especially about how big the subjects are.

the picture was taken in Dubai, at around evening. I am not sure about the size because I didnt want to touch the subject. However surprisingly after 1 hour the spider and its prey was gone.

The pictures don't show the eyes, but from the shape of the cephalothorax, this is a jumping spider. Large ones are about 1 cm long, so unless that moth is huge, the size range fits. Here's a user-submitted picture from spiderid.com showing Platycryptus undatus feeding in a similar way:

Jumping spiders frequently attach a silk dragline to the ground before jumping. This functions as a safety line if they miss, but also allows them to change their position in midair which helps them to land on their feet even on surfaces that aren't parallel to the one they jumped off of.
So, probably the spider saw the moth resting on the wall or wherever, jumped on it and injected venom, the moth dropped from the wall and tried to escape, but the spider attached the dragline to it. Possibly the spider then retreated up the silk line to wait for the moth to die, and went down to feed once the silk line stopped moving, which is when you found it. The picture above came with a comment that the spider ate its prey in-place, so yours probably will not try to move the moth.

I believe the spider was around 1cm long . But after an hour both were gone. I thought it might have fell on the ground cause if you watch the video there was wind blowing from the window, I am not sure how resililent the silk is, but I couldnt locate it in the floor.

Thank you, +1. Fun to learn new things about my favorite kind of spider!


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Relation/difference between metabolism and cellular organisation

In the highlighted paragraph from NCERT textbook, they mention that cellular organisation is the defining property of life forms while metabolism without exception is also the defining property of life forms. My doubt is whether the term 'metabolism' also includes the metabolism reaction in vitro condition too or metabolism only means all the chemical reactions occuring in the cell excluding in vitro condition. If what I mean is true, does cellular organisation and metabolism both mean the same thing? But then again if both are the same thing, metabolism also should be the defining property of life forms, but it is not the case as mentioned by my textbook. So that means both metabolism and cellular organisation are different things. Is this right?

This paragraph appears to draw a distinction between "the sum total of all reactions in cells" and "some isolated reactions that occur in cells". The former is "metabolism" and one defining trait of life; the latter are "metabolic reactions" and can occur in a test tube, and if so they do not fit tidily in a living/nonliving distinction (the paragraph talks about "not living things" but "surely living reactions", which is one way of illustrating the confusion I guess).
As to whether "metabolism" and "cellular structure" are the same thing, I think it's not so much that they're literally the same thing but they're not really separable, are they. The cellular structure is made by "all the chemical reactions in the cell", and "all the chemical reactions in the cell" are mediated by the cellular structure. It's a bit like trying to separate out "a race" from "the people running in the race". You can have one or two metabolic reactions happening in vitro, but if you had all of them in your test tube, happening the same way they do in the cell, you'd have a cell.
The reality of course is that there isn't a single all-encompassing definition of "life", so don't try and nitpick things too much. Metabolism is important because it's what allows living things to do what living things do, thermodynamically speaking. Cellular structure is important because it happens to be the way all living things implement their metabolism, and arguably it is a necessary requirement for metabolism to occur (there are arguments for why you need a small space enclosed by a membrane for example). Other things are also important like reproduction (and other near-universal feature of life that is a basic thing living things do, and allows Darwinian evolution), being subject to Darwinian evolution (because that is the process that leads life to being optimized in the way it is, and able to do the things it does to begin with), sensing and reacting to its environment (all this stuff about "what life does", well, those are universal things life does)... That means you can have arguable examples like viruses, which I would expect your textbook to call "nonliving" because they do not have metabolism or a cellular structure, but some others might call "living" because they have genetic information, replicate, are subject to Darwinian evolution and share a common ancestor with all other known life. The labels are less important than the features one is discussing at any one time. I expect your textbook probably says something like this at some point.

thank you so much!


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The size of the Triceratops specimen Lane in the Houston Museum of Natural Science
In 2012 the Houston Museum of Natural Science published they discovered an almost complete fossil of Triceratops including fossilized skin, see HMNS post, and nicknamed it "Lane".
I am interested to know the size of the Triceratops specimen Lane and in particular: total body length (TBL), total head length including the frill (THL) and brow (superorbital) horns cores length. Estimation of weight would also be great but I doubt if there are any.


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Bite Force of Triceratops
Estimations (or measurements) of bite force is usually conducted for toothy predators like sharks, theropod dinosaurs and crocodiles. For example: Tyrannosaurus had a bite force of about 57 kN (about 5.7 tonne-force) while a 5.2 meters long Saltwater Crocodile (Crocodylus porosus) recorded a 16,700 Newton bite (by Gregory M. Erickson). See my earlier question Reference for the bite force for Nile Crocodile for reference.
However, although paleontologists agree herbivore ceratopsian dinosaur Triceratops had quite a strong bite due to large jaw muscles anchored to (part of) the frill, and sharp hard beak. However, as far as I am aware, no one ever tried to quantify how strong is Triceratops bite. But maybe there are some estimations in paleontological literature and scientific research. So to sum-up my question:

What is the bite force of a fully-grown bull Triceratops?

Size for reference: Triceratops length was 8-9 meters and weighed 6-12 metric tonnes.

these may be helpful https://www.jstor.org/stable/2406631?seq=1#page_scan_tab_contents and https://pdfs.semanticscholar.org/744f/48001115d764d2ff4ad9a47de599900bf531.pdf

A Nile Crocodile bite force was measured to be 5000 lbf (22.24 kN) by Dr. Brady Barr. The bite force of T. rex is about 3 times higher.


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What is the current status of the taxon Crocodylus raninus?
What is the current status of the taxon Crocodylus raninus, the Borneo Crocodile? See Wikipedia Is it now a valid species, a subspecies of Crocodylus porosus (The Saltwater Crocodile) or merely a synonym of the later?
As for Colin Stevenson, "Crocodiles of the World, Reed New Holland 2019", it is not listed as a (valid) species, nor in the IUCN Crocodile Specialist Group.

I started to dig into this a little bit.  I think the answer is probably "it's very uncertain". I don't actually know if there's an official (rather than a scholarly) standard for validity;  I couldn't find anything at https://www.iczn.org/outreach/faqs/ ...


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Are the spikes or prongs in the frill of Ceratopsids considered horns?
Many Ceratopsids, mostly of the subfamily Centrosaurinae, have long spikes or prongs sticking out from the edge of the frill, most famously Styracosaurus, but also Diabloceratops and Rubeosaurus and more. Those spikey projections were almost surely sheathed in keratin, which forms the horns in extant species, such as bovids. Are these frill spikes can be considered horns?