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Clonal selection theory, how does antigen reach lymphocytes?
Clonal selection hypothesis often defined by four basic principles of which first two are

Each lymphocyte bears a single type of receptor with a unique specificity.

Interaction between a foreign molecule and a lymphocyte receptor capable of binding that molecule with a high affinity leads to lymphocyte activation.

If 1) is true and lymphocytes are differentiated to respond only to a specific antigen, the quanitity of lympocytes for a given antigen must be as low as total lympocytes / total antigen receptors. For 2) to happen, the very rare lymphocytes for an antigen must physically touch the antigen.
How is 2) achieved, assuming that 1) is true, and probability theory is a thing?
Edit: This question was heavily critiqued but once more, maybe the reason for that is the wrong reason. What Zhi said in 2019 perfectly reflects my own thoughts about the usual model of immunology, However, one B cell producing only one specific antibody would be unlikely to rapidly find its matching antigen. I do not mind the occassional random person I do not know projecting their prejudice on me, but, again, maybe done for wrong reason?
Shi, Z., Zhang, Q., Yan, H. et al. More than one antibody of individual B cells revealed by single-cell immune profiling. Cell Discov 5, 64 (2019). https://doi.org/10.1038/s41421-019-0137-3

Welcome to SE Biology. Please finish reading the [tour] and consult the help on asking questions. You will see that you need to give evidence that you have tried to answer this question yourself. What texts have you consulted? What you state about the theory (now fact) is incorrect. Each lymphocyte does not “only respond to one antigen”, it only responds to antigens that can bind to its receptor — hence polyclonal antibodies. And if you think something is statistically improbable, you need to present an argument that is at least partly numerical.

This is the role of antigen-presenting cells, which are in charge of carrying samples of antigens to the secondary lymphoid organs (lymph nodes, spleen) where lymphocytes live.
Once activated, B and T cells can activate each other through B-cell presentation and T-cell dependent activation.
It's also important that, for B-cells, the anti-body that they produce is still modified during clonal expansion through affinity maturation. This is essentially very fast mutation and selection that fine-tunes the antibody. So, there doesn't have to be an exact match to begin with, just a reasonably good one that will be improved during expansion.

Thanks. Exact information transmission in immune system is very fascinating. Similar to peer-to-peer networks in computer science, for how two nodes find one another, which is a very hard problem still being worked on. Jerne's original work called it "the immune network".

If antibodies as "packages" exist in 10^17 per milliliter serum, and they can magically connect antigen with lymphocyte through a sophisticated information relyaing mechanism, maybe similar approach can be used for P2P networks actually.

Actually major difference in p2p network is "antigen" wants to be known. So, query flooding requests are likely exactly analogous to antibodies in how they're already being used.


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Glycogenolysis & Gluconeogenesis
Is glycogenolysis and Gluconeogenesis is the same in the terms of product formed?
This doubt arrived when I was attempting true & false and the question was
Glucocorticoids stimulate glycogenolysis, lipolysis and proteolysis
The answer given was false because "Glucocorticoids stimulate gluconeogenesis, lipolysis and proteolysis"

Obviously not from the feedback you received. Have you done an Internet search or consulted Wikipedia. Please do that before posting here.

Hello and welcome A learner,
Glycogenolysis is the breakdown of the molecule glycogen into glucose.
Gluconeogenesis is the metabolic process by which organisms produce glucose and other sugars from non-carbohydrate precursors.
These processes arrive at the same product (Glucose).
Glucocorticoids stimulate the process of Gluconeogenesis but not the process of Glycogenolysis.
To elaborate...
Glucocorticoids are steroid hormones that stimulate production of glucose in the liver via Gluconeogenesis. But Glucocorticoids are not involved in the pathway of Glycogenolysis.
Therefore: Glucocorticoids do not stimulate glycogenolysis, lipolysis and proteolysis.
And the answer is false.

source: Stack Exchange

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Did humans evolve the ability to swim? Or is it just luck that we are able to swim?
Many animals like ducks have evolved features to be able to swim. Even not so aquatic animals like a tiger evolved so that its feet can act as paddles. In humans I don't see any direct feature that has specifically evolved for the purpose of swimming. So is it just luck that we are able to swim and some of our cousins like gorillas are not able to swim? Or did we evolve in some way to be able to swim

I think you have the question backwards.  It'd seem to be more reasonable to ask whether there are animals that CAN'T swim.  I can't think of any offhand: certainly most of those I'm familiar with can.  Some, like dogs, actually enjoy it.

Well, of course, with questions of this sort nobody knows. However before posting you might ask whether there is any reason that the ability to swim has been so advantageous to our ancestors that it has been subject to evolutionary selection. You might also think about the habitat of such ancestors. It is interesting that in fishing communities (e.g. in Scotland) most fishermen had never learned to swim. Why not? Because if your boat flounders in a gale you drown, whether or not you can swim.

@jamesqf oh... I thought there are many animals that can't swim. I know hippos drown in water, but they can maneuver easily and water is their forte, there maybe animals that don't float and may not be able to learn to swim

@David interesting to know. I thought there are some definite traits in humans which show how we evolved to be able to swim, which I don't know, but many people who study these things may know.

@user41965: I don't think there are many.  For just mammals, it seems that the only ones that actually can't swim are giraffes: http://www.bbc.com/earth/story/20170320-the-cruel-experiments-that-revealed-most-mammals-can-swim  (I suppose you could argue about whether what hippos do in the water actually counts as swimming.)  The difference seems to be that with most mammals, swimming is pretty much instinctive, while with humans & other great apes, it has to be learned - even if, as in my case, the learning was a matter of the bigger kids pushing you into the deep part of the creek :-)

The Jane Goodall website says: "You’ll rarely see a chimp paddling about in the water as they don’t like to swim. Their low body fat ratio causes them to sink and their top heavy body composition makes it difficult for them to keep their heads above water.  However, some chimpanzees do enjoy a good splash around in shallow water."
Some monkeys have been taught to swim, see this video: https://www.youtube.com/watch?v=q2vekGuV8xA
So, the answer is, it's just luck that humans are quite good swimmers compared to other monkeys, because strong bipedal running and legs also gives humans good stability in water. After us the best swimmer is the proboscis monkey. Many other monkeys do play in water and swim: https://www.youtube.com/watch?v=sn-M1kCvzLg
There are many studies that theorize that modern humans have evolved beside seas and rivers.
Here's a massive infographin on the subject: https://visual.ly/community/Infographics/science/possible-aquatic-adaptations-human
Humans crossed the open ocean at least 50,000 years ago, i.e. to colonize Australia, the oldest evidence of fishing is currently from East Timor, 42,000 year old fishing hooks: https://www.livescience.com/17186-oldest-fish-hooks-early-humans.html#:~:text=Their%20discovery%20uncovered%20fishing%20hooks,%2C%22%20O'Connor%20said.

I was also thinking the same, the fat and size of our lungs can be attributed to our energy needs.  Which are probably not meant for swimming, but I'm guessing they play a role. I've heard theories about the reason we lost body hair may be due to living in seas. Of course water is the source of life and it makes sense that humanity thrives near water bodies. But I don't see any features in humans (that I know of) that have evolved to make swimming easier. But such an important skill like "swimming" just being our luck and not evolution.. I mean, what're the odds, Idk...

I put some other evidence of monkeys swimming, It's interesting the difference between baboons who swim and run very well like dogs, and big forest apes like chimps which swim completely differently.

@com.prehensible however the way each kind of ape/monkey is swimming, I think the main reason we're able to swim (as long as we don't have paddles) is because we're able to float reasonably well and we can put our nose out of the water while maintaining the position. Now that I think of it, and I've searched and found this link news.com/biology/science-chimpanzees-orangutans-swim- maybe many animals can swim, but maybe they just don't learn to do it

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Is it a trichoderma?
I have got some fungi on a polypore. Can it be a trichoderma?

It certainly could be, given how prevalent they are, but fungi are nearly impossible to identify visually like this. You need to look at its microscopic structure, run various biochemical assays, and ultimately do sequencing, just like with bacteria.

There are fungal morphologists but they do require microscopes.  some penecilia also have this color... they are also very common... :)

The green colour is darker than I see with fresh Trichoderma infections. It looks like an old infection. My experience limited to growth on coffee grounds and cocopeat.


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Does immunity to CRISPR proteins limit their effectiveness?
The use of crisper-cas systems is currently applied to cells cultivated in vitro. As control of the ‘off target’ effects of Crispr improves and Crispr is used in vivo, why won’t the immune system neutralize it?

Usually not.  the Crispr/Cas proteins can be delivered to the cell as DNA/RNA and the proteins will only exist inside the cell in low numbers.
Even in systems that deliver the protein from the outside in vivo almost always the proteins would be encapsulated in a delivery system to ensure they and any necessary accompanying nucleic acids get into the cell. Getting Crispr/Cas into a cell is difficult to do and they don't just pop in by themselves. They also require guide RNA, which will not easily stay whole in the blood stream and tissues for long.
if you want to just inject a fluid into the blood with unprotected CRISPR/CAS proteins, an immune reaction might stop them.  Not all proteins produce an immune reaction. Sometimes just 2-3 proteins of an entire bacterium produce an immune reaction (antibodies).   But then again its unlikely the proteins would have edited any genomes in any host cells even so.


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What is this organism?

Link to GIF on imgur
What is this flat organism? It is around 1 cm long. I find them in places which aren't cleaned often. Location is India. Are they harmful or poisonous?
Edit: I've found that this is a duplicate question of What insect is this? (India).


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How can I extract ligand with neighboring protein atoms from PDB with complex?
I'm not familiar with biology and coming from Data Science field, so please excuse me for the lack of knowledge. What I want is to create 3D voxel representation of ligand atoms with neighboring part of the protein (looks like it is called pocket) from PDB file which contains complex.
For example, let it be 10gs from RCSB (https://files.rcsb.org/download/10GS.pdb). For other example, it can be 4xit or 4wkc.
What I planned, was identify both protein and ligand atoms, compute the geometric center of the ligand, and then calculate proximity for each atom and fill some 3D surrounding cube.
When I open PDB for this complex (10gs) I see what I understand as two possible binding sites for ligand VWW, and another two - for MES:
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE VWW A 210
REMARK 800
REMARK 800 SITE_IDENTIFIER: AC2
REMARK 800 EVIDENCE_CODE: SOFTWARE
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE VWW B 210
REMARK 800
REMARK 800 SITE_IDENTIFIER: AC3
REMARK 800 EVIDENCE_CODE: SOFTWARE
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE MES A 211
REMARK 800
REMARK 800 SITE_IDENTIFIER: AC4
REMARK 800 EVIDENCE_CODE: SOFTWARE
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE MES B 211

How can I proceed from this point? Does this PDB contain atoms for ligand VWW, properly oriented, and how can I identify them along with neighboring ones of target protein?
Or my formulation of the problem is totally wrong?

You might find RCSB's Guide to Understanding PDB Data and the PDB file format documentation useful. I'll go over some of the information present in PDB files that seems relevant for you, using your example of 10GS.
Ligands are specified in the heterogen section:
HET    VWW  A 210      33
HET    MES  A 211      12
HET    VWW  B 210      33
HET    MES  B 211      12
HETNAM     VWW L-GAMMA-GLUTAMYL-S-BENZYL-N-[(S)-CARBOXY(PHENYL)
HETNAM   2 VWW  METHYL]-L-CYSTEINAMIDE
HETNAM     MES 2-(N-MORPHOLINO)-ETHANESULFONIC ACID
FORMUL   3  VWW    2(C23 H27 N3 O6 S)
FORMUL   4  MES    2(C6 H13 N O4 S)

These records tell you the identity of the ligands that are bound to the protein (VWW and MES), how many are bound (4 in total), the chemical name (in the HETNAM record) and chemical formula (FORMUL record). The HET record also gives the number of associated HETATM records (33 for VWW and 12 for MES). Here are the first five HETATM records for VWW of chain A:
HETATM 3265  N   VWW A 210      15.088  10.798  23.547  1.00 14.90           N
HETATM 3266  CA  VWW A 210      15.010   9.987  24.792  1.00 20.92           C
HETATM 3267  C   VWW A 210      16.115   8.924  24.830  1.00 21.55           C
HETATM 3268  O   VWW A 210      16.520   8.515  25.940  1.00 17.16           O
HETATM 3269  CB  VWW A 210      13.635   9.327  24.908  1.00 14.23           C

Each HETATM record corresponds to an atom in the ligand and gives the chemical coordinates for each on the X, Y and Z axes. For example, the first record specifies a nitrogen atom at coordinates (15.088, 10.798, 23.547).
The connectivity (ie covalent bonding) between atoms in a ligand is specified in CONECT records. Here are the first five from the PDB file:
CONECT 3265 3266
CONECT 3266 3265 3267 3269
CONECT 3267 3266 3268 3273
CONECT 3268 3267
CONECT 3269 3266 3270

This tells you that atom 3265 (the first nitrogen in the HETATM records above) is bonded to atom 3266 (a carbon). Atom 3266 is bonded to atoms 3265, 3267, 3269. Et cetera...
The atoms of the protein are specified in ATOM records. Like the HETATM record, these records give some identifying information (atom serial number and type, residue name and number, etc) as well as the coordinates in 3D space. For your purposes, it sounds like you can just loop through the atoms of the protein and find the ones which are within some threshold distance of an atom in a ligand (or the geometric centre of the ligand). However, this PDB file does already contain some information about the binding sites for these 4 ligands in the SITE records (here are the first four corresponding to site AC1):
SITE     1 AC1 15 TYR A   7  PHE A   8  ARG A  13  TRP A  38
SITE     2 AC1 15 LYS A  44  GLY A  50  GLN A  51  LEU A  52
SITE     3 AC1 15 PRO A  53  GLN A  64  SER A  65  TYR A 108
SITE     4 AC1 15 HOH A 229  HOH A 303  ASP B  98

The SITE records also have corresponding REMARK 800 records (which are given in the question). For example, site AC1 is described as BINDING SITE FOR RESIDUE VWW A 210 as identified by SOFTWARE. So in this case, these SITE records are a list of residues that make up the binding site of their respective ligands.
You may want to be somewhat wary of these SITE records because (1) as far as I know they are not mandatory records in a PDB file and therefore may not always exist, and (2) it is not entirely clear how they are generated. In this case they are software generated... but which software... or what algorithm? I have previously looked through the SITE record of a binding site in a protein I am very familiar with and noted some conspicuous absences from the list of residues, so take that for what it's worth.

Thank you very much! I think I can proceed from this point. Yes, I've already found that SITE records are not mandatory while collecting ligand ids. For example, they are absent in 1f4x, 1hge, 4c4r, etc.

You have perfectly answered my question! But can I please ask you one more theoretic question which arises when I look into this data? There are two ligands for 10gs complex on RCSB, and there is affinity value (Ki) for only one of them - VWW. But even VWW is binded in two places already. How can I possibly understand it? I think it will be incorrect if I will completely forget about MES and will treat each of two binding sites of VWW with the same Ki value, right?

@Slowpoke MES is actually a buffer used during the crystallization of the protein. While it may bind the protein with some affinity, it isn’t really a ligand so much as an artifact of the experiment.

As for VWW binding sites: the protein is a homodimer and both binding sites are identical. Barring some kind of cooperative binding, the affinities should be the same.


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Suspensory ligaments: why are they ligaments?
Don't ligaments connect bone to bone? In the eye for example, the suspensory ligaments connect the ciliary muscle to the lens, which obviously aren't bones. Is this just one of those instances where the terminology isn't that precise and you just have to memorize the exception?

you are thinking of articular ligaments, those connect bone to bone there are a lot of other types of ligaments. suspensory ligaments support many different organs.

"...The suspensory ligaments connect the ciliary muscle to the lens..."

You must be referring to the Zonule of Zinn (Such a great name).
You are absolutely correct, the definition of Ligament varies across texts which can create confusion.
For example:
Merriam-webster:
A tough fibrous band of tissue connecting the articular extremities of bones or supporting an organ in place.
Wikipedia:
A ligament is the fibrous connective tissue that connects bones to other bones.


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DNA denaturation and Renaturation
If we denature dsDNA by heating it and then rapidly cooling it then what would happen?
I read this question, where it was written that if we were given dsDNA sample which was completely denatured and then if we rapidly cool it. What would the result be? Would it anneal rapidly too or the annealing will be slow?

If we see PCR the annealing time varies but is around 45 sec min with temperature range from 55-65 °C ( depending on Tm value). So my first doubt is that is it called rapid cooling?
In case of preserving the RNA or DNA- cooling on ice pack preserves its structure and prevents any further changes in structure also.
I tried to read papers and I read somewhere thatif we completely denature it then it anneals slowly. That takes place in two steps- first, it will try to find its completely match by collision process. Second, it will zipper up. That takes around 55 mins. So that states that it will be rapid annealing.

“I read this question” Where? Is it some sort of homework or test question. Are you sure this has anything to do with PCR? Could it be a basic question that has been used for the last 50 years and merely relates to the effect of temperature — low, medium and high on the hybridization interactions?

How long of a DNA molecule are we considering? For short fragments like in routine PCR, the collision process and annealing will occur much quicker than 55 min. What temperature is it annealing at? Think of it like molecule kinematics....

To denature something can have different meanings:
In context of dsDNA it means separation of the 2 stands, while the individual strands themselves are fragmented.
I assume your question addresses PCR. In this context, rapid cooling to very low temperatures would prevent annealing of the two separated strands.
Other than that I want to point out a common misconception, that rapid cooling somehow has 'destructive' effects, which is not true. The more rapid something is frozen, the better it's structure is preserved.

But in PCR the primers are of short length, that means it would anneal rapidly as, annealing in that case is primer attachment. If I consider a complete ds DNA which would again anneal. That might be a long strand, so that would probably take more time?

A long strand takes more time. Also lower temperatures don't automatically mean faster annealing. There is an optimal temperature around 50C, where far below that the reduced molecular movement actually reduces the annealing speed.

It really depends on a variety of factors. (1) the nature of the dsDNA, is it a plasmid or chromosomal DNA? Plasmids more easily renature than chromosomes, so rapid cooling and heating my not affect renaturing of plasmids, but affect DNA.
Cooling it slowly in some PCR-based experiment may be done if you want to annealing DNA fragments but are not sure about the optimal annealing temperature. Commonly done if you want to anneal two primers together for example. You need to be more specific so we can help you out.

I have edited my question. Can you check again?


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Transformation of coordinates found in PDB
According to the PDB guide there are some coordinate translation matrices found in PDB file:
ORIGXn                  Transformation from orthogonal  coordinates to the
                        submitted coordinates (n = 1, 2, or 3).
SCALEn                  Transformation from orthogonal coordinates to fractional
                        crystallographic coordinates  (n = 1, 2, or 3).
MTRIXn                  Transformations expressing non-crystallographic symmetry
                        (n = 1, 2, or 3). There may be multiple sets of these records.

For example, in 10gs complex from RCSB I see:
ORIGX1      1.000000  0.000000  0.000000        0.00000
ORIGX2      0.000000  1.000000  0.000000        0.00000
ORIGX3      0.000000  0.000000  1.000000        0.00000
SCALE1      0.012543  0.000000  0.001805        0.00000
SCALE2      0.000000  0.011055  0.000000        0.00000
SCALE3      0.000000  0.000000  0.014557        0.00000
MTRIX1   1  0.945333  0.099229  0.310644       -5.48795    1
MTRIX2   1  0.099832 -0.994906  0.013998       21.83043    1
MTRIX3   1  0.310451  0.017779 -0.950423       27.67516    1

I want to do 3D voxel reconstruction of some part of the complex stored in PDB. What is the purpose of those matrices, do I need to apply any of those translations to the coordinates stored in PDB to "standartize" the data and obtain the same coordinate system and same grid for different PDBs? Or they are just related to the data which was submitted by authors and are needed for inverse translation? Or something else? Thank you very much!

The purpose of these matrices is to reconstruct the crystal lattice from the coordinates, which only contain one copy of the repeating structural unit found in the crystal. In other words, they represent the affine transformations required to convert one copy of the repeating unit to its neighbors.
To a biologist (as opposed to a crystallographer), these are not useful except if one of the crystallographic symmetry axes happens to also be a biological dimer (or other multimer) axis. However, in this case, the PDB usually gives an option to download the "biological unit", which includes the coordinates for all neighboring copies that associate in the cell with the copy specified by the original coordinates. I should point out that sometimes the biological unit is in fact smaller than the crystallographic unit, if multiple copies of a monomer or dimer or whatever occur in non-equivalent spatial contexts within the crystal. There is no substitute for biological knowledge to know what the relevant structural unit in the cell is.

Thanks! So, it means that generally I can forget about them and treat different PDBs from RCSB as represented in the same coordinate system and use spatial representation of those different proteins as data points for training a machine learning model (e,g, classifier) without any recalculation?

Different PDBs from RCSB? There is no way to relate the coordinates frames of entirely different proteins that are not bound to each other in the same crystal, their rotational and translational positions are arbitrary because they aren't relative to anything. There is no such thing as the "top", "bottom", "back", or "front" of a protein. Only distances and angles, i.e. measures within the internal coordinate system of a molecule, are meaningful. If you mean the length scale, then yes that's the same across all PDB files (it's always in units of Angstroms).

Okay, so we may consider that coordinate system across PDBs is the same up to orthogonal transformation (rotation, swap of axes, etc). Scale is always the same and is represented in angstroms, angles are preserved. Thank you!


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Strange planarian/leech like creatures found with California blackworms
I've been trying to ID these things myself but to no avail.  They came with a shipment of California blackworms from Florida.  I've heard so many ID's and apparently it's not uncommon to get these kinds of flatworm like hitchhikers with blackworms, but apparently different suppliers have different hitchhikers, so what one layman claims they are doesn't necessarily apply to another supplier.
I've heard these guys are planarians, leeches, or some sort of parasite specific to blackworms. I can probably eliminate most of these guys, but I just noticed they gave "birth" or something.  I thought they reproduced via fragmentation, but I saw one with what looked like legs, and realized it was actually dozens of smaller babies wiggling underneath.
I'm worried, because I don't want them to kill my blackworms, or accidentally kill my fish.
The creatures are about a half an inch stretched out? the creature is inside of a standard 3ml pipette in the later pictures. They tend to wiggle back and forth (see the video). They scrunch up into a small ball when I disturb them.

It's hard to tell because they are transparent, but the below gif is definitely the same type of creature.   Basically half the time I see them, they stick their heads out of the water and wiggle back and forth like that (but not sway, like the blackworms).   My phone isn't good enough to capture this behavior well.

https://i.stack.imgur.com/I9v24.jpg

Welcome to Biology.SE! You need to upload individual images (e.g. files ending in .jpg). I expect the problem you are having is that you are trying to upload your entire page of videos and images, which this system wont do. Each image in imgur has a separate url that must be individually uploaded. If you want to include information from videos you need to capture stills from that and then upload them. HTH

@tyersome All the images are too large, and in linking it claims that the images are not the right format.  I also have no idea how stills then uploading works?

(+1) Glad you got the images figured out! Can you provide some additional details about what we are seeing in the final gif? It looks to me like an entirely different type of organism ...

@tyersome It's hard to tell because they are transparent, but it is definitely the same type of creature.   Basically half the time I see them, they stick their heads out of the water and wiggle back and forth like that (but not sway, like the blackworms).   My phone isn't good enough to capture this behavior well.

Wild — I hope someone comes through with an answer for you. If you don't get an answer here you might want to try iNaturalist, which specializes in identifications. If you do get an answer there please post an answer here to your own question so others can find it in the future. Good luck!

@tyersome Thanks for that link!  I found bigger versions and more of them, hopefully I'll be able to get better pictures.


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Any kind of online "molecular modeling playground"?
I'm wondering if anyone has ever made a tool to try out new molecular modeling/simulation algorithms, where the tool itself handles the "boring" tasks of loading PDB files, building chains of amino acids from sequence so that the atoms can later be assigned coordinates by user scripts, rendering rotatable graphics in 3D, etc., but where the user can then write scripts that loop over the coordinates, do some kind of math, and then modify the structure. That way you could experiment with new force fields, integrators, etc. Something like TurtleToy does with plotter graphics.
There are obviously molecular modeling tools with scripting capability, but quite a few have licensing restrictions and also they are commonly intended as ways of splicing together existing algorithms and modeling "recipes" in new sequences. The actual simulation code is often "buried" deep in complex codebases and spread across multiple files that must be compiled together just to get something working. Clearly something like an energy minimizer written in for loops in a language like Python won't compete in terms of speed with GPU-accelerated parallelized C++, but it can be written completely from scratch to test out completely new algorithms, and if seamlessly integrated with a rendering component that accepts redraw calls from in the script, it's a quick way to visualize "what is this doing to my protein structure?" in real time as you single-step through your algorithm (and the rendering overhead probably makes speed a moot point there anyway). That way if you want to quickly see "how does my method compare to the existing ones in CASP" or something, you have a "playground" to try it out.
If I'm looking for this I'm sure others have too, so I'm wondering if it exists. An even potentially more interesting feature would be the ability to execute scripts as "filters" over the PDB, something like "Find all sequences of length 5-20 amino acids in the PDB for which this expression evaluates to "True", align them using the following transform, and plot them in this canvas". But I can see where the PDB might not like people doing this as it could bog down their servers from all the fetches, so this may be a bad idea. But allowing people to operate on their own PDB files would obviously not be a problem if the tool were around.


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Myelinated vs Un-myelinated
If an axon is completely myelinated (doesn't even have Nodes of Ranvier), is it faster than an un-myelinated axon when conducting action potentials?

What do you think would happen in an axon without nodes of Ranvier?

The action potential would die out without any further stimulus, right?

Yes. So..what's the conduction velocity of something that doesn't conduct further?

Would the velocity be 0? And would that mean that the un-myelinated axon is faster?

Does it matter how fast a train is if it never gets to the destination? I wouldn't say the velocity is zero, it's meaningless.

Ok, thank you for explaining


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Rigorous definition of the kinship coefficient and proof of a recursion thereof
I am reading Section 5.2, Kinship and Inbreeding Coefficients, of Kenneth Lange, Mathematical and Statistical Methods for Genetic Analysis. There the kinship coefficient $\Phi_{i,j}$ is defined for two relatives $i$ and $j$ as the probability that a gene selected randomly from $i$ and a gene selected randomly from the same autosomal locus of j are identical by descent. Then the book states that suppose $k$ and $l$ are the parents of $i$,
$$\Phi_{i,j}=\frac12(\Phi_{k,j}+\Phi_{l,j}) \tag1$$
with some exceptions.

Equation (1) seems intuitive. Yet it is slippery for a proof especially considering the exceptions. The root cause is that the definition of $\Phi_{i,j}$ is vague albeit seemingly plausible. I am seeking a mathematically rigorous definition of $\Phi_{i,j}$ and a proof for Equation (1) together with the condition under which it applies.

The definition as set by Kenneth Lange's book is indeed quite vague and thus unrigorous. It is a probability not conditioned on observing an allele $a$ at a locus of $i$ but conditioned on the following where we focus on one particular locus. It is rigorously defined as follows. Then we will give the correct formulation of the correct recursive equation akin to Equation $(1)$ which is in general wrong.

A graph of lineage contains nodes, which we call persons, of a particular locus. Each node, or person, contains exactly two genes. We draw one and only one directed edge (parental relationship) from a gene of a parent person to the gene of a child person if the latter is inherited from the former.  This is a directed acyclic graph (DAG). Each gene can be connected by no more than $1$ edge directed to (as opposed to away from) it. The two genes in one person cannot be connected by edges. Two persons are said to be connected if there is an edge pointing from a gene of one node to a gene of the other node. Two persons cannot be connected by more than one edge. For a pair of connected persons and their directed edge between them, the edge is equally probable to connect to one gene as the other gene of a person, i.e. the probability is $\frac12$. A pair of genes (persons) are said to be connected if there exists a undirected (simple) path from one gene (person) to the other. Two connected genes are called identical by descent.
In this setting, the DAG with respect to the persons is given and deterministic whilst any directed edge in the DAG assigned to two persons are random with independent probability $\frac12$ with respect to the genes within each person.
For a pair of persons on a lineage DAG that is connected, the probability of one gene equally probably chosen amongst the two genes of one person being connected, or identical by descent, to one gene equally probably chosen amongst the two genes of the other person is the coefficient of kinship.
As an additional assumption, the genes that are connected have to be the same and thus assume the same allele.
Definition: Suppose a lineage DAG is given. Let the kinship coefficient between person labeled $1$ and person labeled $2$ be $\Phi(1,2)$.  Denote the set of parents and children of person $1$ each of which is on an undirected (simple) path between $1$ and $2$ as $S_2(1)$.
Lamma: Denote the set of paths through an ordered persons $p$ in that order as $P(p)$. $\{P((1,i,2))|i\in S_2(1)\}$ partitions $P((1,2))$.
Proposition: $$\Phi(1,2)=\frac12\sum_{i\in S_2(1)}\Phi(i,2).$$
Note: The summation in the Proposition is over $S_2(1)$ rather than the set of all parents and children of person $1$. That fixes the condition under which Equation $(1)$ is valid.
Corollary: $$\Phi(1,2)=\sum_{p\in P((1,2))} \frac1{2^{n(p)}}$$
where $n(p)$ is the number of persons on path $p$. $n(p)=|p|+1$.


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Can birds pass diseases to humans through contact surfaces?
My friend asked me the following question. She has a pigeon nesting on her window and the pigeon often touches the window, and my friend also sometimes touches the window (e.g. open and close it). The question is does the touching of her and the pigeon in a common surface (the window) can transmit infections or disease from the pigeon to herself? Is there a risk letting the pigeon nest on her window pane?

But it's on the other side of the window?! So how is that the same surface?

Provided she washes her hands after touching surfaces that came into direct contact with the pigeon, there shouldn't be any relevant health risks from touching this surface.
And just because it sound like the pigeon somehow is nesting WITHIN her apartment: Be aware that pigeons can carry mites that could spread within the apartment and infest plants. I would advise against having wild pigeons in the apartment!
EDIT:
Knowing the pigeon is outside, it's not 100% necessary to remove the nest. It depends on whether this window is used for venting and on the direction of air pressure. (does wind go in or out at this side of the house?). Also it depends on the visual cleanliness of the nest. Bird-droppings can potentially represent a health risk, as they can spread through the air, once they dry out, while potentially containing dangerous micro-organisms. Same with feathers that lie around.
So if wind regularly comes from the side of the nest, she could remove the nest for safety reasons, especially if the window is in the kitchen. Otherwise she can't overcome that guilt by blaming health.

Thank you for your answer. The pigeon is nesting on the outer window pane and not inside the apartment. Is the risk of mites still relevant?


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Bed bug or booklouse?
I found this creature climbing on the lower part of a wall inside apartment. Can you distinguish if it's a bed bug nymph or a booklouse? Sorry the photo quality isn't great, because it's so small (2 mm). Thanks in advance!

See Insect identification - Is this a bedbug? for more information about bed bugs

After looking it up, I can, with some confidence, confirm that this is a book louse in the larval stage, as seen in this picture:
https://bpca.org.uk/write/MediaUploads/Pages/A-Z/Booklice/booklice-1.jpg
I hope this answers your question!

you should add a link about bedbugs to ilustrate the difference of the two species.https://en.wikipedia.org/wiki/Bed_bug


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Why are the pulmonary vein and artery not like the rest of circulatory system?
I'm learning anatomy. What I learnt is that we have arteries that have oxygenated blood which appears red in color, and branch blood to arterioles to deliver blood to cells via capillaries from where de-oxygeneated blood is collected via venules into veins to go back for oxygenation. So:

artery = oxygenated
vein = de-oxygenated

However, in defining the pulmonary vein and pulmonary artery, I see the reverse of these definitions.
The pulmonary artery is for de-oxygenated blood.
Why is it so?

Ask youself, what function is served by pulmonary circulation? What function is served by systemic circulation? What part of the anatomy connects the two?

It is true that nearly all arteries carry oxygenated blood and nearly all veins carry de-oxygenated blood, but that is not what defines them. Arteries are blood vessels that carry blood away from the heart, and veins carry blood towards the heart. If you look at the situation in that light, the naming makes sense: the pulmonary artery is carrying de-oxygenated blood away from the heart to the lungs, and the pulmonary vein is carrying the re-oxygenated blood back to the heart, to be pumped through the rest of the body.

Although these complicate classification.


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Can severe vasoconstriction increase systolic blood pressure?
I know that, vasoconstriction results in increased total peripheral resistance which is responsible for the rise in diastolic blood pressure. Also, cardiac output is responsible for the systolic blood pressure. But there are conditions, as in administering nor adrenaline, where there is severe vasoconstriction and a fall in cardiac output but a rise in both systolic and diastolic blood pressure. In this case, I understand that the rise in diastolic blood pressure is due to vasoconstriction produced by nor adrenaline. I am not able to account for   the rise in systolic blood pressure in the setting of falling cardiac output. Can severe vasoconstriction also influence the systolic blood pressure?

Yes. Imagine you're blowing into a balloon. Your airflow into the balloon represents 'cardiac output'. As the balloon gets larger and larger, the pressure inside the balloon (the 'peripheral resistance') rises, and the amount of air you can blow in ('cardiac output') falls. Your systolic and diastolic BP both rise. Does that make sense?

Yes I understand, I had come to a similar conclusion. Thank you for confirming it.

'Total peripheral resistance determines diastolic pressure, cardiac output determines systolic pressure'—what is the source of this statement? In what context was it made?

Highest pressure measured in an arterial pulse pressure trace, systolic blood pressure, is during the systole of the heart, so it is the cardiac output responsible for this whereas the lowest pressure in an arterial pulse pressure trace, diastolic blood pressure, is maintained by the tone of the blood vessel (total peripheral resistance). This is my understanding.

@souravthampan Hmm, that does not look like a very sound argument. Nor is this statement supported by any experimental evidence (as far as I know).

I think the heuristic 'total peripheral resistance determines diastolic pressure, cardiac output determines systolic pressure' is not a good one after all. E.g., it does not explain the effects of norepinephrine. Nor does it explain the phenomenon of age-related change in blood pressure: see https://www.ahajournals.org/doi/full/10.1161/01.cir.96.1.308. Part of the reason is, it does not take into account vascular compliance, which has a major role in determining pulse pressure.


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What is the very hard sphere inside the eye of many common fish made of and how is it called?
Inside the eye of many common fish, like tuna, scad, snapper, actually probably all fish I have eaten, is a small sphere made of some very tough substance. This sphere is even hard to crush with teeth, and seems to be made of homogeneous material. That is after the fish is cooked, not sure how it is uncooked. It is immersed inside a quite soft, almost liquid substance inside the eyeball.
Is that the lens, or is the whole soft semi-liquid tissue the lens?
What substance is the small tough sphere made of? I imagine some type of proteins, but what type of proteins exactly?

From what you describe, it seems the hard sphere is the lens and the semi-liquid substance is the vitreous humour. Like the lens of other vertebrates, the fish lens is made of lens fibres—cells rich in proteins called crystallins.
For more on the anatomy of fish eyes, you could read this page and watch this dissection video.


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Why severely increased Ligand (eg Hormones) concentration downregulates the Receptor?
As an example continuous high blood level of GnRH in humans causes a suppression of LH and FSH. This is due to the fact that increased GnRH downregulates GnRH-Receptors . My question is how this is done and why? What are the probable molecular mechanisms underlying this effect?

Kumar P, Sharma A. Gonadotropin-releasing hormone analogs:
Understanding advantages and limitations. J Hum Reprod Sci.
2014;7(3):170-174. doi:10.4103/0974-1208.142476
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229791/

Hi A.N. Ψ, Could you provide more resources on continuous high blood level of GnRH in humans causes a suppression of LH and FSH? Or on the fact that increased GnRH downregulates GnRH-Receptors?

Go through the paper. I have added it to the Question

Gonadotropins are hormones synthesized and released by the anterior pituitary gland, which act on the testes and ovaries to increase the production of sex hormones and stimulate production of either sperm or ova.
The hypothalamus contains Gonadotropin-releasing hormone (GnRH). Intermittent released of GnRH is responsible for the biosynthesis and secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland.
LH stimulates interstitial cells to release testosterone, which triggers spermatogenesis. The rising level of testosterone exerts negative feedback control on the hypothalamus and pituitary glands.
GnRH has been shown here in a negative feedback loop
This feedback loop has great interplay with the number receptor levels as you suggest.
(From a quick search) I found one paper (behind a paywall) that states the following information when studying rats:

We observed an acute reduction of both GnRH and GnRH-R mRNAs 24 h after the injection [of GnRH agonist (triptorelin)] (about 38% of control).

Transcription does not equal translation, but it seems that acute increased levels of GnRH cause a reduction and mRNA of GnRH and GnRH-R and therefore potential reduction (down-regulation) of protein levels of GnRH-R.


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Identification of a red arachnida (?) (picture and video)
I found this in a greenhouse in Norway. It is a few millimeters in size, I could fit 5-6 of them on my thumbnail.

It looks a lot like this one from Wikipedia https://en.wikipedia.org/wiki/Trombidiformes
Can someone help me identify it? Is it a parasite or a harmless creature?
Also a video of it moving around
https://1drv.ms/v/s!AlmW2TG6jr_7ga4eTDLz7qzKM4W_8w
Update:
I found a link description which makes me think it is a mite (same as the Wikipedia link).

One of the most common sources of confusion between ticks and mites is color. No known species of naturally occurring red tick exists. But ticks can sometimes appear to be red if they’re in the act of feeding. However, the spider mite, red velvet mite, clover mite and the larvae of the harvest mite—known colloquially as chiggers—all take various shades of red.

It might also be a type of predatory mite -- these are frequently used in organic or IPM agriculture to control spider mites. See for example this wikipedia page. I would talk to someone at the greenhouse and see whether they release predatory mites.

looks like a tick to me

@aminabzz I thought it looked like a tick as well, but I have never heard of red ones or seen a description of one. Going to update the question with a reference regarding that.

it is clover mites here is a video about them: https://www.youtube.com/watch?v=BftGk-S2GyU


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Does the coast of California support a larger population of marine mammals than Maine?
Visiting the Maine and California coasts, I've noticed that it is much more common to see marine mammals from the coast in California, including seals, dolphins, and whales. I've been hypothesizing about reasons that this might be the case, and have come up with several ideas.

I'm a tourist, not performing a formal population study. Maybe the numbers are similar, but my measurement method is flawed. I've looked up some better numbers in the NOAA Stock Report:

Seals:

Harbor seals, Maine (75,000) vs. California (27,000),
California Sea Lions, California (257,000).

Whales:

Gray Whales, California (27,000)
Humpback Whale, Maine (900) vs California (15,000)

Dolphins:

Common Short-Beaked Dolphin, Maine (170,000) vs California (839,325)

There are many other species, but these numbers seem to confirm that California has a larger population. Of course, the coast of California is also much larger than the coast of Maine. I'm not sure how to correct for that.

Maybe the fishery in the North Atlantic is more overfished. Wikipedia says that 71% of fish capture comes from the Pacific vs 20% from the Atlantic, but that the Pacific has only twice the volume of the Atlantic[1]. This is much more general than California vs Maine coast, but it suggests that the Pacific has a larger fish population than the Atlantic per volume which could support a larger mammal population.

Maybe there are more protected habitats in California. 15% of the south coast region is protected from fishing. Whereas in Maine, I was able to find information about proposed Marine Protected Areas, but no information about currently protected areas.

Does the coast of California support a larger population of marine mammals than Maine? If so, what factors support the larger population?

You might consider the California coastal current as one possible factor: https://en.wikipedia.org/wiki/California_Current

Assigning whales to a particular coast seems particularly difficult given the large territories that many (most?) species associate with

Also why limit to Maine? There's nothing particularly special about Maine vs, say, New Brunswick and Newfoundland and Nova Scotia, besides political boundaries

@BryanKrause Maine is simply the location where I have visited the coast. If you would prefer to answer for a larger section of the North Atlantic coast, please do.

@BryanKrause NOAA fishery stock report specifically assigns Humpback Whales in the Gulf of Maine as a "relatively  discrete  subpopulation(s),  fidelity  to  which is determined matrilineally"


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What are all the possible developmental stages an insect can be in?
I'm making an app which allows the user to report insect observations. Many bugs may exist in different forms throughout their life time. For example, a butterfly will exist as an egg, a catterpillar, a pupa and lastly as a butterfly. A greenshield bug can live as a nymph and then as an adult.
I want to make one list that contains all morphological stages that insects can be in. Then the user can select the appropriate one for the species he or she observed. My question is: What are the names of these stages? Are there any other stages next to the egg stage, caterpillar/larval stage etc?
Thank you

This process is refereed to as Metamorphosis, is a biological process by which an animal physically develops. Furthermore, Animals can be divided into species that undergo complete metamorphosis ("holometaboly"), incomplete metamorphosis ("hemimetaboly"), or no metamorphosis ("ametaboly").
Otherwise there is the process known as Holometabolism, which more specifically pertains to insect development. This process defines almost all the types of insect development.
Others include: Ametabolism and Hemimetabolism.

can a nymph also be considered a holomatebolic stage?

A nymph is the immature form of some invertebrates, particularly insects, which undergoes gradual metamorphosis (hemimetabolism). So unfortunately no.

The stages are called instars:
https://en.wikipedia.org/wiki/Instar
It changes depending on the insect: it can be caterpillar, grub, maggot, 2nd instar, 3rd instar, larval stage, larva, eruciform, scarabaeiform, campodeiform. Here are some pages:
https://entomology.ca.uky.edu/ef017


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Why don't moles repair their DNA?
Cells have mechanism to repair damaged DNA. So why don't the cells in moles (the spots), repair themselves and the moles dissappear?

What makes you think that moles are caused by DNA damage? Please cite the source of this information.

@David because people get moles from sun damaged skin. So I put 2+2 together.

Let's try again. Are you asking why the known mechanisms of repair of e.g. UV damage to DNA are not 100% efficient, or are you thinking that the DNA repair mechanisms somehow detect that the DNA has been changed in the mutated cells (e.g. the transformed skin cells) and can reverse this ("repair themselves")? If all mutations got repaired there would be no evolution.

@David Let's not.

As is appropriate for a comment on a question that is unclear and lacks detail, I asked for clarification on specific points. If you had made this clarification I would have attempted to answer your question. As you refuse to do without giving any reason I have no option other than to vote to close.

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. However it is yet to be linked closely to mammalian moles.
Information here, states:

"Moles are overgrowths of skin cells called melanocytes, but the genetic factors involved in their development are not well understood."

The BRAF gene is one of the most well-studied genes involved with benign moles, if a mutation arises in this gene - there may be a production of an altered protein that causes melanocytes (melanin-producing cells located in the bottom layer of the skin's epidermis) to aggregate into moles.
I cannot answer why DNA repair does not occur. Maybe the cell cannot identify the mutation, maybe the cell cannot corrects the damage, or maybe it is also from environmental factors. This is an active area of research, but receives far less attention compared to cancer or heart disease.


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Can the eye determine which type of defocus is presented to it?
I have a question regarding myopic and hyperopic defocus.
My question is, is the eye able to determine which type of defocus is presented to it and if so what mechanisms allow it to distinguish between the two types of defocus. This question was thought of after reading a study which showed that the eye's AL could change temporality based on which type of defocus was presented to it and I was unable to find a definitive answer on to why this happens.
As well as this, I saw numerous reports on how different lenses can slow the progression of myopia by presenting peripheral myopic defocus onto the retina without an explanation on why this occurs.
Thank you for taking the time to read my question and I look forward to your response!


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Action potential attenuation in unmyelinated axons vs demyelinated axons
I learnt that action potentials travel much faster along myelinated axons, and when these axons are demyelinated the action potentials travel much slower and sometimes die out. Why do action potentials die midway in unmyelinated axons?

In unmyelinated axons, there are voltage-gated ion channels along the entire length of the axon. Depolarization in one segment depolarizes and opens ion channels in the adjacent segment, which further depolarizes the next segment, etc.
Myelinated axons are built differently. They have stretches of myelinated axon which are (mostly) free of voltage-gated channels, interrupted by nodes of Ranvier that lack myelin but have dense voltage-gated channels. The depolarization at one node has to be sufficient to reach the next node for the signal to propagate.
Normally this is no problem. Thanks to insulating myelin, the signal propagates unattenuated for a long distance. However, if you start to lose myelin then some of the signal is lost along the way (specifically, the current goes to charge the membrane capacitance, which is reduced by myelin) and it may not be enough to open voltage-gated channels at the next node of Ranvier.

Myelinated axons have schwann cells around them, electrically insulating the neuron axons except for gaps in the sheath which are called the Nodes of Ranvier. The insulation increases the speed of transmission of action potentials.

Without myelination conduction signals along the nerve can be impaired or lost.
There are some diseases E.g. Acute disseminated encephalomyelitis where myelination is lost.


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Do identical twins have the same metabolism rate at birth?
Will monozygotic twins defecate at the same time if fed at the same time during the first weeks of life?
They should have the same genetics (and epigenetics) since they are monozygotic and the same environment since they live in the same house and they are just born.
I looked if metabolism (assuming it is correlated to defecating) is a genetic trait. I found this review about basal metabolism of infants but it stated that the methods aren't good and not comparable.
If there is no information for humans, what about other mammals?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, questions should be clear and narrowly scoped (i.e. answerable in a few paragraphs rather than needing an entire book). To be clear you need to say what you mean by "metabolism". I would say that most humans have the same metabolism since with rare exceptions we all possess the same suite of metabolic enzymes. However, that has nothing to do with intestinal transit times, so you must mean something else. ...

...  ——— Note that we also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

At the first year of my biology teacher program in university,a professor wrote on board "x=/x"(x isn't identical to/same as x) to indicate the difference of individuals no matter how much they look the same. Monozygotic twins have identical DNA and hereditary characters, but the bodies that are formed under the guidance of the DNA aren't identical.

@Harun could you elaborate? In plantsI learned that somatic clones are assumed to be identical in any aspect since the rate of rando mutations, transposone jumpings etc. is relativley small and causes no significant difference at the start

Do identical twins have the exact same gut flora? Does exposure to the same environment produce the same gut flora? Is there an element of randomness in there?

yes, genetic trait. thank you. I guess they will have. I learnt that most of the microbiome of a child comes from his mother and the rest from the (same in this case) environment. There will be randomness but will it be significant?

@Hachiloni How exactly does a baby's gut flora come from the mother?

@RodrigodeAzevedo - Partially & Hachiloni, yes it would be significant. Microbiota greatly influence metabolism.

I like admire your interest.
Organisms in development rely not only on their genetic make-up but also: their environment and epigenetics (no matter how early in development).
In addition to variables other than the ones stated...
In reality if we were to test this - the twins wont eat at the same speed, expend the same amount of energy, stay the same temperature, eat the same amount, or drink the same amount as each other.
With so many extraneous variables, it leads one to believe that it is very unlikely identical humans or other organisms would defecate at the same time.
I can direct you toward some (no-pay wall) literature on the Nature/Nurture debate or Twin studies.

thank you for the answer. As far as I know identical twins should have the same epigenetics and environment initially, that's why we do this kind of experiments on them. I understand from your answer that this is a too difficult to answer question. I would dig into the literature you posted.

Epigenetic patterns are similar, but not the same between identical twins. Well environment is not even true, they may not always be together and so it is again, similar but not the same. It would take small amounts of carcinogens to dramatically alter results. I am sorry this isn't the answer you like. But it is the best answer available.

I meant a too difficult to answer scientificly as there are many uncontrolable variables. Not that you answer wasn't a good fit for my question. Apologies if I wasn't clear

Not too difficult to answer scientifically. Even if we tried as stated above in my answer - it is highly unlikely. Does that not answer your question? It does. But it's not the answer you wan? You cannot get SE members to solve arguments for you.

They should have the same genetics (and epigenetics) since they are
monozygotic and the same environment since they live in the same house
and they are just born.

https://childrenswi.org/medical-care/fetal-concerns-center/conditions/infant-complications/twin-to-twin-transfusion-syndrome

If untreated, the survival rate for TTTS twins is approximately 10 to
15 percent.

So in your scientific opinion, that whole website and condition is just pure garbage, and the parents and doctors are making it all up, right?
Because of course twins always have the exact same metabolism?
Do you have the scientific integrity to admit your conclusion here?

I think I mentioned I'm not a animal biologist but a plant scientist so I don't know all the possible syndromes. Obviously this condition will make identical twins non-identical and therefore they are excluded from my question.
Your comment seems agressive. And, from the comments and answers I got this sites seems too agressive and oversensitive to be a good place to ask questions


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Why do beta-1 and beta-2 adrenergic receptors result in two completely different effects (though both use Gs pathway)?
$\beta_2$ adrenergic Receptors are $G_s$-coupled 7-TM proteins. Considering that $G_s$ , by activation increases $[\text{cAMP}]_\text{cytosol}$ which inhibits MLCK of smooth muscles (and causes relaxation as in bronchial smooth muscles).
But at the same time, in cardiac myocytes ($\beta_1$), $G_s$ activation activates PK-A (through cAMP) which in-turn activates L-type $\ce{Ca^{2+}}$ channels. Thus there is prolonged plateau phase and positive inotropic and chronotropic effect.
I think these two results are contradictory. Why and how are these two seemingly completely opposite effects mediated through similar signal transduction pathways?

Madamanchi A. Beta-adrenergic receptor signaling in cardiac function
and heart failure. Mcgill J Med. 2007;10(2):99-104.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2323471/

The autonomic nervous system is composed of the parasympathetic and sympathetic nervous systems. The sympathetic nervous system is stimulated via adrenergic receptors.
Adrenergic receptors are G protein-coupled receptors stimulated by norepinephrine (noradrenaline) and epinephrine (adrenaline).
There are 4 sub-types of adrenergic receptors:

Beta1-adrenergic receptors
Beta2-adrenergic receptors
Beta3-adrenergic receptors
Beta4-adrenergic receptors

Yes, Beta2-adrenergic agonists reduce bronchial Smooth muscle contraction.
Yes, Beta1-adrenergic agonists increase heart rate.
Here we can see activation of different tissues from different receptors, that activate the same pathway. Thus, despite the example explained - the activation of the same path-way - different responses ensue.

In the human airway - Smooth muscle cells express Beta2-adrenergic receptors the most (100%).

In human heart tissue (Cardiomyocytes/Cardiac muscle cells), of Beta-adrenergic receptors - Beta1-adrenergic receptors are expressed the most (75–80%).

"...the cAMP pathway generally promotes contraction in cardiac muscle; however, in Smooth muscle, activation of cAMP causes relaxation."

Source
cAMP inhibits myosin light chain kinase, the enzyme that is responsible for phosphorylating Smooth muscle myosin and causing contraction. Thus no contraction takes place in smooth muscles cells.
Inhibition of myosin light chain kinase increases intracellular cAMP, which further inhibits myosin light chain kinase thereby producing a lower contractile force (E.g. promoting relaxation).
Source


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Why does Cyan appear bluish rather than greenish, when the phototopic eye sensitivity is highest in green (and Cyan contains blue and green equally)?
Cyan contains blue and green equally.
Phototopic eye sensitivity is highest in green.
Why, then, does Cyan appear bluish to most of us, rather than greenish?


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How to construct a sgRNA library with multiple samples?
I was wondering if anyone has already experience with constructing sgRNA libraries. We are interested in doing a knock-out experiment (loss-of-function) with 5 different conditions.
I have found this protocol from Joung et al.
In the protocol they have 10 different Fwd primer with no unique barcodes, only the eight Rev primers contains unique barcodes for different samples in KO.
Do I understand it correctly, that I can pool together only eight samples in one sequencing run with this protocol?
I would like to better understand the protocol of constructing an ngs library for sgRNA samples. If someone can point me to the right link/page?
Are there more complex library preparation kits out there which can deal with more samples?

Hi @AssaYeroslaviz, the question you are asking is wet-lab question on CRISPR rather than a bioinformatics question. You could consider posting on Biology SE if this is the consensus here. The design of a CRISPR construct is a Bioinfo SE question, rather than wet-lab protocols in my opinion


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Why do we have both on and off bipolar cells?
I have a question regarding the reason behind the 2 bipolar cells.
So, from my understanding we have both on and off bipolar cells and from the numerous diagrams I have seen, I find that most show a single cone attached to both an off and a on bipolar cell.
The on bipolar cell reacts in an inhibitory manner to glutamate and so if light hits a photoreceptor attached to this bipolar cell, less glutamate is released and so the bipolar cell will become depolarised.
The off bipolar cell is the opposite as it finds glutamate to be excitatory and so it will become depolarised in the dark.
My question is, in the light if a single cone has light presented to it, it will become hyper polarised and so will release less glutamate. If the bipolar cells attached to this cone have opposite effects as in one will become depolarised and one will become hyper polarised what is the reason for the off bipolar cell, why would we need that cell if it only becomes depolarised and doesn't result in anything?
A second question is, do the bipolar cells connect to corresponding ganglion cells for example, on bipolar cell connects only to on-centre ganglion cell? If so why is this?
Lastly, we also have single cones that connect to single bipolar cells. Are these cells on or off bipolar cells I assume they are on because if they were off we wouldn't be able to sense anything as the cell would be hyper polarised and so wouldn't cause the ganglion cell to reach an action potential. Is this thinking correct?


text:
Which amino acids can be phosphorylated?
Definitely serine, tyrosine, and threonine. What about aspartate and glutamate? I thought the O- on the carboxylic acid side group could be phosphorylated but am getting mixed responses to this. Any thoughts / any other amino acids I'm missing?

Also check out the relevant wikipedia page. For "homework" questions, you are required to show your attempt to answer the question and to use the "homework" tag. (Note that "homework" can apply to questions even if they are not assigned as homework — for example those that are trivial to biology professionals and thus easily answered by searching.) ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I don’t see why it is suggested that this is a homework question. Most readers will not know the answer, and if there happens to be a resource that has all that information it may not be obvious to the poster. If either of those who have commented are able to provide a comprehensive answer which puts the topic into perspective, they should do so. The question is not posed in a very academic manner, but it can always be improved upon. A mere list is clearly of little interest.

There's a Wikinome page called Phosphorylation of unusual amino acids describing phosphorylation of histidine, aspartate, cysteine, lysine, and arginine. Lysine and arginine are apparently phosphorylated on the nitrogens. I was a little surprised to see histidine and aspartate on the list, as histidine kinases seem to come up often in my area of research.
I'm also aware of at least one non-proteinogenic amino acid, creatine, which is phosphorylated by a dedicated creatine kinase. It functions as a sort of phosphate shuttle for rapid regeneration of cellular ATP from ADP in situations of high metabolic demand.
References:
Phosphorylation on unusual amino acids. (http://kinase.com/wiki/index.php/Phosphorylation_on_unusual_amino_acids)
PubMed Abstracts: https://pubmed.ncbi.nlm.nih.gov/?term=18558627%2C10772951%2C10698688%2C1654322%2C9553104%2C8577821%2C19498169%5Buid%5D
Guimarães-Ferreira L. Role of the phosphocreatine system on energetic homeostasis in skeletal and cardiac muscles. Einstein (Sao Paulo). 2014;12(1):126-131. doi:10.1590/s1679-45082014rb2741


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Can you still contract a disease after being vaccinated and be able to spread it?
I assume I know the answer to this already but wanted to confirm before I respond to someone that appears to be arguing that vaccines don't make you immune (they only stop your symptoms?) - but you remain infectious?:

She also doesn’t realise that if a vaccine works like she believes then the vaccinated would have less symptoms which in result offers more chance of spreading it. literally how covid spreads so fast now. “no or mild symptoms“ to most. Thats the sole reason it spreads so fast. So technically getting vaccinated is more dangerous in spreading disease than someone that gets sick and stays at home.

Edit: This question is about vaccines in a more general scope as that was the discussion at hand, but if anything it would be more closely targeted at COVID-19, which I'm aware there is currently no vaccine for.
My understanding of vaccines in general is that they don't technically make you "immune", but they make you immune to the effects of the virus, because your body will already know how to beat it.
But in saying that, my assumption has also been that because you have somewhat of a immunity to it then if you get "infected" with the disease you aren't contagious to others.
Additionally, I assume getting "infected" with the disease and being protected against it's effects is different to being asymptomatic - both have no symptoms, but you are still truly infected with it if asymptomatic and can still pass it to others, it's just not affecting your body enough to give you symptoms.
Just thinking now, but if your body knows how to fight it off already, then maybe you are truly immune to it - just because it enters your body doesn't mean it infects you right? Your body knows how to fight it off before it does. Like, an attacker can enter your grounds and knock at the door, but your guards know how to fight them off before they enter the area of your grounds where they 'cause the trouble'.
...but on the case you CAN get infected with it, but it doesn't present any symptoms, are you still contagious to others?
Additionally, I'm not talking bout virus shredding here from getting a vaccine, I know all about that.
One would think the proof is in the pudding in that many diseases have all but been eradicated from the world because of some vaccines, but I argue with myself that if vaccines don't make you immune then perhaps these diseases have only largely seemingly been eradicated because most everyone has been vaccinated (with vaccination preventing you from the effects only, not getting infected?) - thus only appearing on the surface they have been eradicated, but they are still around, but just don't pose a health risk to those that are vaccinated?
So, primary question is, what is meant exactly by "immunity", can you still contract the disease and if so would you still be contagious to others?

It would really depend on what kind of vaccine/disease you are referring to, as it there is a substantial amount of variation in the immunity they offer. Could you clarify your question?

@4galaxy7 I have edited my post. It was more in a general nature of how vaccines work, but I have clarified a little.

I tried to break down your question into smaller parts and answer them individually:
Q. What is immunity?
A. Simply put, immunity is the ability to react to an infectious agent and stop it from causing disease.
Q. Do vaccines make you immune to infectious diseases?
A. Yes, by definition. If it doesn't make you immune, it's not a vaccine.
Q. Can we get disease even after being vaccinated?
A. Yes, because no vaccine is 100% efficacious. For example, the MMR vaccine has about 97% efficacy in preventing measles.
Q. Do vaccines prevent infection?
A. It depends on how the vaccine works. Some vaccines enable the immune system to actually reduce survival and multiplication of the infectious agent. The polio vaccine is an example$^1$. It leads to generation of antibodies that neutralise the virus$^2$.
Other vaccines prevent disease (or reduce its severity) but do not prevent infection. The diphtheria toxoid is a good example of this$^3$, because the antibodies generated by vaccination neutralise the toxin while leaving the bacterium unscathed. (I believe all toxoids behave like this.)
Q. Can we spread infection even after getting vaccinated?
A. Yes. This is easy to see for those vaccines (like diphtheria, mentioned above) that prevent disease but not infection.
Vaccinated individuals can spread infection with the other, multiplication-stopping kind of vaccines too. Again, this happens because no vaccine is 100% efficacious. Note that chances of spread are reduced (as compared to the unvaccinated scenario), even if they are not zero. For instance, see the work of Seward et al$^4$ on breakthrough varicella.
Q. The big question: is getting vaccinated more dangerous than not getting vaccinated?
A. Sorry, but this is not the place to discuss it. It requires a careful look at the risks and benefits of vaccination, not just for the individual but also for the community at large. That would be a discussion more appropriate for Medical Sciences Stack Exchange.
To summarise: yes, we can catch a disease and spread it even after being vaccinated. The chances of this happening vary with the kind of vaccine.

Journal articles cited

Howe HA. Am J Public Health Nations Health. 1957 Jul;47(7):871–5. https://doi.org/10.2105/ajph.47.7.871
Faden H, Modlin JF, Thoms ML, et al. J Infect Dis. 1990 Dec 1;162(6):1291–7. https://doi.org/10.1093/infdis/162.6.1291
Miller LW, Older JJ, Drake J, et al. Am J Dis Child. 1972 Mar;123(3):197–9. https://doi.org/10.1001/archpedi.1972.02110090067004
Seward JF, Zhang JX, Maupin TJ, et al. JAMA. 2004 Aug 11;292(6):704–8. https://doi.org/10.1001/jama.292.6.704

Suggested reading

https://www.who.int/health-topics/vaccines-and-immunization
https://www.ncbi.nlm.nih.gov/books/NBK27131/

Another factor is diseases like influenza, where the virus has a very large number of variants, and vaccines are effective against only some of them.  (Which is why there's a new influenza vaccine, or vaccines, every year.)

Thank you for your information answer. Couple questions - So with vaccines such as the diphtheria one, is it safe to say that you can spread it in much the same way as if you had the disease? Secondly, you state that the other kind of vaccines you are still able to spread it because no vaccine is 100% efficacious; so basically you're saying you CAN'T spread it if the vaccine has been effective (as you won't get infected), but in the small percentage that it isn't effective then THAT'S when you are still able to spread it - because you will then thus be infected?

@Brett 1. Yes, vaccinated persons with adequate immune response can spread the diphtheria bacillus (as described in journal article 3 above). 2. Yes, in the other case it's the people who do not respond to the vaccine that can spread the infection. But many other factors are involved, like organism load, herd immunity, etc.

Thanks again. With regards to vaccines like the Diphtheria one, as you state you can still spread it as it only prevent against disease, not infection; but a secondary question on that, when getting the vaccine is there any worry about spreading it FROM the vaccine itself, as in do these types of vaccines contain the live virus or would it just be similar in fashion to "virus shedding" from vaccines where some contain weakened versions of a live virus and the only concern to others around you is generally only immunocompromised people?

@Brett For diphtheria in particular, there is no risk of infection with the vaccine itself as it is a toxoid (an inactivated toxin). On the other hand, live attenuated vaccines work by CAUSING an infection. If your immune system is functioning normally, the infection is mild/asymptomatic and gets cleared quickly, and this creates immunologic memory. But if the immune system is weak, these vaccines can be dangerous because they may cause severe infections.

The WHO vaccine safety course is a good place to learn about the different types of vaccines and their safety profile: https://vaccine-safety-training.org/.

Great - thanks for all your help. :)


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Can a second mass extinction by microbes happen?
Science Daily reports that the mass extinction at the end of Permian period happened by the Methanosarcina archaea wiping out 90% of species:

Methane-producing microbes may be responsible for the largest mass extinction in Earth's history. Fossil remains show that sometime around 252 million years ago, about 90 percent of all species on Earth were suddenly wiped out […]. It turns out that Methanosarcina had acquired a particularly fast means of making methane, and the team's detailed mapping of the organism's history now shows that this transfer happened at about the time of the end-Permian extinction.

Is it possible by the global warming and all the spores of bacteria come out from melting glacier or anywhere else and mass extinction occur?

Worth considering that when reasons for a mass extinction are investigated the answer is often "All of the above", because anything that changes the environment contributes. we have for instance also found massive volcanics and a massive impact crater at the same time.

The first problem here is that the theory that the P-T extinction was caused by bacteria (rather than bacteria being a possible effect/feedback) is contradicted by LOTS of evidence, primarily the Siberian Traps eruptions igniting large coal beds.

First of all, let’s consider your Methanosarcina scenario in specific.
Methanosarcina with those properties are still around. So, there is no reason to expect that introducing some ancient Methanosarcina into a suitable environment today would do very much – as they should already be there. Any existing (large-scale) environment providing a niche for Methanosarcina should already be occupied by it as it only needs a single organism to get there by chance at some point.
Moreover, there must be some reason why our atmosphere stopped being filled with methane by Methanosarcina.
For example some prerequisite resource could have been depleted, some other organism evolved that consumes this methane or controls the Methanosarcina population by feeding on it.
Whatever this reason is, we should expect that it still applies: A required resource would still be gone and a second organism controlling this activity should still be around (or resurface together with the Methanosarcina in question).
In fact, the hypothesis you mention maintains that the nickel required by Methanosarcina to produce methane was available in huge amounts due to specific volcanic activity at that time.
Finally, the current ice masses of the Earth are much younger and have not been around since the Permian period.
In general, if geologically cryostoring microbes were relevant, climate change should be the least of our worries as drilling a hole into the ice or local geologic activity could suffice to bring back a few individuals – which is all that would be needed.
Now, what about unfreezing microbes in general?
Due to lack of fossils, we have little knowledge about microbe extinction, except that it does happen.
However, my ecological intuition is that microbes either lose their niche to a fitter alternative (which either be more apt at causing problems or avoid them resurfacing) or survive in small amounts (ready to occupy their niche if it should resurface).
Microbes are considerably different from higher, sexually reproducing life forms here as it only needs a single individual to revive the species and individuals can survive for a long time in adverse conditions, not only by sporulation but also because they need little energy to maintain their state.
Finally, if a niche for disastrous microbes exists, there is the constant risk that it will be filled by some ordinary microbes evolving, which brings us to the next point.
Something that is conceivable to happen is that some microbes spontaneously evolve to fill a big niche and have some disastrous by product leading to a mass extinction.
It is hard to estimate this risk, but as far as I know, there is no historic precedent after the evolution of higher life forms.
(As elaborated above, the Methanosarcina hypothesis for the Permian extinction features additional factors.)
However, I consider it unlikely that climate change increases this risk.
While climate change undoubtedly has disastrous ecological consequences, tilting individual ecosystems, I don’t see how it creates some fundamentally new environment (that wasn’t already there in similar form somewhere else on the planet) that would stimulate a spontaneous disastrous microbial evolution.

"a fitter alternative (which would be even more apt at causing problems)" I think I've heard specialists mentioning that being fit, for a microbe, entails not causing too many problems.

@bli That is only true for microbes that live inside another organism and depend on it to stay alive.

@jpa: Not necessarily.  Consider for instance a microbe that produces oxygen as a waste product, but can't tolerate high concentrations of environmental oxygen.  So as the Great Oxygenation Event gets under way, those microbes either mutate to tolerate oxygen (with the intolerant dying in large numbers), or they become extinct.  Or consider yeast fermentation: at some point the yeast produces an ethanol concentration that's toxic to them.

@jamesqf: Well, if we have something like the great oxygenation event, the oxygen producing microbes were fitter as far as the answer is concerned. More generally, my point is if microbes go extinct, it is because their niche is taken by some other species, which should either increase the problems (if the niche has gone too and then re-emerges) or voids them (because the dangerous microbes have no niche to go to). Also see my edit.


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Is there a metric for “evolutionary agility”?
By "evolutionary agility" I mean how fast an organism can adapt to changes in the environment. I’d imagine that a population with more offspring and a shorter time between generations would be more “evolutionary agile”.

Yes, there is a measurement laid out by Haldane (1949) called 'Darwins'. One Darwin is given an $e$ fold change in a trait over the period of 1 million years.
As to your second point, yes there are different variables which control the rate of adaptation within a population. The classic factor is genetic variation, as given by Fisher's (1958) fundamental theorem of natural selection, which states:

The rate of increase in fitness of any organism at any time is equal
to its genetic variance in fitness at that time

So broadly speaking, individuals with more additive genetic variation will adapt more rapidly.
Of course, there are many other factors such as generation time, effective population size and mutation rate will influence the response to selection. However, such as in the case of generation time, the relationship is not necessarily a simple one (Gandon and Mikalakis, 2002).
EDIT
After re-reading your question, I think I perhaps misunderstood it.
I suppose the term you are looking for is 'evolutionary potential', which is defined by Steeves et al (2017) as:

The capacity of a population to evolve in response to environmental
change.

There is a nice chapter in this book which gives a good overview of the topic. The chapter may perhaps be available for free on certain websites.
References

Haldane, John Burdon Sanderson. "Suggestions as to quantitative measurement of rates of evolution." Evolution (1949): 51-56.
Fisher, Ronald Aylmer. The genetical theory of natural selection. Рипол Классик, 1958.
Gandon, Sylvain, and Y. Michalakis. "Local adaptation, evolutionary potential and host–parasite coevolution: interactions between migration, mutation, population size and generation time." Journal of Evolutionary Biology 15.3 (2002): 451-462.
Steeves, Tammy E., Jeff A. Johnson, and Marie L. Hale. "Maximising evolutionary potential in functional proxies for extinct species: a conservation genetic perspective on de‐extinction." Functional Ecology 31.5 (2017): 1032-1040.

Even things like what form of reproduction it uses can be an influence, sexual selection can both speed up and slow down the spread of genes for instance.

Of course - this being biology there are an infinitude of variables which can influence the rate of adaptation - too many to include in a short post!


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Why are Chromosome Territories important?
Chromosomes occupy discrete regions of the nucleus, referred to as 'Chromosome Territories'. This spatial organization is emerging as a crucial aspect of gene regulation and genome stability in health and disease.

But how is this the case when:

Most eukaryotes seem to have Chromosome Territories, but yeast S.
cerevisiae is an exception to this.

So if some eukaryotes do, and some do not, what information do Chromosome Territories provide? Some literature uses the phrase 'non-random chromosome territory arrangements'. Thus, I am confused.
Chromosome territories are randomly arranged in some eukaryotes.
How are chromosome territories crucial for gene regulation and genome stability in health and disease in some  eukaryotes, but random in other eukaryotes?

First, this idea was discredited or ignored during several decades, some studies suggest that CT is random in some eukaryotes that isn't necessary the truth. It is not easy at all to determine is CT are random or not
Second, not all eukaryotic organism are the same. Plants and Fungi have cell walls, animals do not. Fungi can have a dikaryotic cell or even undergo somatic hybridisation.
Third, "chromosomes are more unfolded in lower eukaryotes such as yeast."Chromosome Territories: The Arrangement of Chromosomes in the Nucleus
This article does not mention that S. cerevisiae is an exception, on the contrary "and may even hold for single-cell eukaryotes, such as budding and fission yeast".
Thank you for the question, I learnt a lot while searching for an answer


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Does bone resorption cause alkalosis?
The phosphate in hydroxyapatite Ca5(PO4)3(OH) is a strong base, PO4^3-, and the hydroxide is also a base, OH-. I was talking with a biologist the other day about if bone resorption (at a level that causes elevated calcium and phosphate) also causes alkalosis. He did not think so, but mentioned that it might be buffered or compensated for. In general, does bone resorption cause alkalosis?

I'm not sure if this helps but Metabolic alkalosis decreases bone calcium (in general).


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Function of amatoxins
There are a couple of papers and "lots" of anectodal evidence which imply that mushroom hunting does not have any adverse effects on the fungi, neither short nor long term. One of the counter arguments for that is that some fungi developed deadly toxins and what reason do they have other than stoping animals from eating them?
So, I had this discussion recently and I raised this point. I was told that many compounds that fungi produce do nothing for the fungus and they are producing them just because they are not costly enough to be cut by evolution. I don't find this argument particularly compelling, so I was wondering whether we know anything about the function of such compounds, say amatoxins.
Do they have any function other than killing us? Are they used by the fungus for anything during its life cycle? Do they kill insects or larvae? Do we know anything about them?

I think this is a great question with minimal research in this area. There are superagonists that bind to human receptors better than our endogenous ligands. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4813425/


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Coronavirus: Why does soap inactivate the virus on skin, but not on surfaces?
In a comment on "Stability of SARS-CoV-2 in different environmental conditions", published today in The Lancet Microbe, it is stated that household soap is highly effective on the skin. Not much further down the same paragraph it is noted that soap cannot be used as a surface disinfectant for SARS-CoV-2.
So why is it so effective on hands, but so ineffective on a sink?

Are you sure that's what the comment actually says?

Can you please cite the paragraph which states that?

In the third paragraph it says, "The virucidal effects of different disinfectants on SARS-CoV-2 were investigated with a number of incubation times (eg, 5, 15, and 30 min), and no infectious virus could be detected in all cases with the exception of a 5-min incubation with hand soap."

My question is meant as "why is soap effective on the hands, but not on surfaces". Perhaps it is due to different modes of application between washing and disinfecting. One involves constant friction, the other just exposure.

Where does it say anything specifically about the effect of disinfectant on SURFACES?

The entire subject of the research, the paper and the comment is the stability of the virus on surfaces in various conditions.


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Why do we get tunnel vision during fight or flight response?
I have a question regarding tunnel vision during the fight or flight response. I believe that during fight or flight high levels of adrenaline are released which causes the pupils to dilate allowing more light to enter which allows us to be more aware of our surroundings. Why is it that sometimes we suffer from tunnel vision then? I know it allows us to focus on the main threat but if our pupils are dilated and more light is entering and hitting our retina how is it that we have tunnel vision? Shouldn't we see more now with a dilated pupil?
Thank you for reading my question!


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What would happen if we place denatured DNA in acidic medium?
DNA can be denatured at high temperatures or in alkaline solutions. But DNA can be annealed at low temperatures. I want to ask, could it be annealed in acidic medium?

Hello and welcome Nandini Yadav,
It is worth mentioning DNA is an acid (Deoxyribonucleic acid) and intracellular pH is most commonly between 7.0 and 7.4.
Alkaline reagent Example

"The sodium hydroxide (NaOH) is a commonly used reagent to denature the DNA by increasing the pH. At an alkaline pH, OH- groups are predominant. They remove the hydrogen- bonds-contributing protons from guanine and thymine, thus breaking the hydrogen bonds between the two oligonucleotides."

Source
You can see in the image below hydrogen bonds between nucleotides Adenine (A), Cytosine (C), Guanine (G) and Thymine (T).

Acid reagent Example

A decrease in the pH was found to deteriorate the thermal stability of DNA

Source
At an acidic pH, the H+ in the surrounding environment of DNA is high and therefore the hydrogen bonds between Adenine (A) and Thymine (T), Cytosine (C) - Guanine (G) will 'break'.
More information here.


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Do babies have a fight or flight response?
Do babies react in the same way as young children and adults in regards to the fight or flight response? If they do not respond in a similar way or don't have a fight or flight response at all then at what age is this developed. My teacher said that babies don't have a fight or flight response and we are unsure of when this develops but I'd like more information if there is any.
Thank you!!

I think it is 6 months of age, however I found minimal supporting information.


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What type of white hard thing grows on lobster
I have no idea how to explain it. It looks like mini white volcanoes growing on a lobster shell.  Is it bacteria or parasite?

These are barnacles, which are interestingly related to lobsters. See the image for comparision (from here):

They have a mobile larval stadium, but once they mature, they attach to a hard surface. They can be found on ships, surfaces in harbours, on whales and obviously on lobster shells. See here and here for some more details.

ah, even more creepy in your up-close image!

The question also asked if they were parasitic - do they do any harm to the animal in question? Given that lobsters are food animals, would the lobster be safe to eat?

@nick012000: It's arguably a form of parasitism, since the barnacle gains (a surface to attach, and one that is usefully mobile for defence and food collection) whilst the lobster loses by having to carry the barnacles, and appears to have no benefit. But it is a surface contamination only, and AFAIK the types of barnacle pictured are harmless to us on outside of food, they can simply be ignored or removed. There is a different barnacle that has evolved to feed on the host directly - https://theconversation.com/the-crab-castrating-parasite-that-zombifies-its-prey-27200

There's a Disney movie waiting to be written about Larry Lobster and his frenemies Barry, Bill, Bud, and Barney Barnacle.


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How is Elysia chlorotica classified as an animal capable of photosynthesis?
Elysia chlorotica is a kind of sea slug. Technically, it's an animal. However, it undergoes a process called kleptoplasty, which is the absorption of chloroplasts from algal prey cells which are then used to produce food. E. chlorotica uses these chloroplasts for 9-12 months at a time, and manages to keep them functioning. Also, E. chlorotica has absorbed some algal genes, however, none are related to photosynthesis, and none are expressed.
So, Elysia chlorotica is a sea slug that is capable of photosynthesis, but only after taking chloroplasts from its prey.
What I'm wondering is how do you classify something like this? I know E. chlorotica is currently listed as a mollusc in kingdom Animalia, but what if it fully absorbed its preys genome and was able to sustain chloroplasts on its own? Would E. chlorotica be considered a plant or an animal? Or something else? Is that even possible?
I know this is a lot, and maybe this forum isn't the right place for my questions, but any insight would be greatly appreciated!

This is a nice question, and has wider implications for phylogenetic classification in general.

Maybe you are familiar with the endosymbiotic theory which hypotetisays that the mitochondria (and chloroplast) was a little procrayote that got absorbed by larger organisme. At the beggining they were independent in an endosymbiontic relationship but in the process of evolution they merged to one organism from which all eukaryotes (plants). So yes, the process your describe is possible.
If it happens than the new organism is no longer E. chlorotica but a another which evolved from it, this creatue will likely still be clasified as an animal since there are non-photosynthetic plants and there are photosynthetic non-plants (algae, cyanobacteria), Therefore photosynthesys is not the definition of a plant.
The goal of the tree of life is to draw the "familiy tree" of all the living creatures. So, if we know one creature is an animal that gave rise to another one with a special ability we will still clasify it as an animal.

A little issue with this answer: what definition of 'plant' are you using? Whittaker (1969) used the term to mean 'multicellular photosynthetic eukaryotes'. Are you using it in a different sense here?

Also, this answer seems to be opinion-based. Citing sources could make it better.

@Adhish: But there are numerous example of plants that have lost the ability to photosynthesize, becoming either parasitic or mycotrophic: https://www.fs.fed.us/wildflowers/beauty/mycotrophic/whatarethey.shtml  But they are plants because they descended from plants that did photosynthesize.

@jamesqf The author has referred to algae as 'non-plants', which is why I raised the question. (PhyloCode avoids terms like 'plants' and 'algae' altogether. The clades relevant to this discussion would be Archaeplastida, Viridiplantae, etc.)

@Adhish plants evolved from algae but they are not plants as far as I thought. Plants belong to the Plantae kingdom and algae belong to the Protista. PhyloCode is not widely accepted nor excluding of other systems. A source: https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Book%3A_Introductory_Biology_(CK-12)/08%3A_Protists_and_Fungi/8.05%3A_Algae

Phylogenetic classification—which has come to be widely accepted—classifies organisms based on ancestry. Evidence for common ancestry exists at various levels: molecular, cellular, tissue/organ, and whole organism structure. It is by synthesising information from all of these that we draw conclusions of descent, and therefore of classification. Thus there is nothing wrong with classifying E. chlorotica as a mollusc: it has this strange chloroplast phenomenon, but is a bona fide mollusc in other ways (see this article).
But what if, as your question says, E. chlorotica actually integrates genes from its prey into its own genome? (By the way, this has already been reported.) Will it still be a mollusc? Or will we need to place it closer to Vaucheria, its algal food?
This highlights a major limitation of the 'tree of life' concept: the inability to take horizontal gene transfer (HGT) into account. Some biologists have come up with other ways of thinking about evolutionary history—such as a 'web of life' or 'ring of life'—to overcome this.


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Can viruses be reintroduced to humans from ice sheets?
A comment on reddit mockingly say

because the ice is melting away due to global warming, this new virus came out of the melted ice sheets

It has 60+ upvotes and no one replied
Is it possible for viruses that are frozen in ice sheets to reinfect humans when they are melted?

Yes, pathogens have been shown to survive freezing temperatures under ice and still remain potentially dangerous after the melting of ice.
This has not only happened for relatively simple molecules such as the ones that viruses are made out of, but it has also even happened with larger pathogens such as bacteria (anthrax outbreak in 2016).
Unlike high temperatures which can cause molecules to dissociate due to excess kinetic energy, freezing temperatures usually preserve molecules and even cells such as with the aforementioned anthrax outbreak. This means that viruses can survive cryogenesis.
In 2015, researchers in Tibet discovered 28 'new' species of viruses in (melting glaciers).
These sort of discoveries lead many to believe that with global warming, previously unknown viruses could appear once again.
As for SARS-CoV-2, it seems that melted ice sheets are unlikely to be the source of such a virus considering (among other reasons) that the virus was first noticed in Wuhan China, a place lacking permafrost.