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Difference between haemocoel and coelom
I am looking for an embryological perspective on the following question.
I know about coelom derivation, but I want to know how haemocoel is derived and how it is fundamentally different from coelom.
True coelom is formed by the cavity formed in mesoderm. It is lined by mesothelium on both sides, whereas on the other side pseudo coelom is cavity which is lined by endothelium and mesothelium. However, the formation of haemocoel is not clear to me.
I have looked for in many books, but I have not been able to find an embryological perspective and what happens to coelom in which haemocoel is present.

I was looking for the same thing and i found the answer in the anatomy of molluscs
you can clearly see that coelom is different from haemocoel and coelom is greatly reduced.
Haemocoel is a pseudocoelom it is a body cavity but not lined with mesoderm at all sides

Ca you add the source (website) of the image and add references to your answer?


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Copy number deletion and high expression
I have a region that has significant CNV loss. But the expression for the genes in those regions is high compared to the expression found in the samples that don't have the regions lost. How can this happen?

Welcome. Please provide some more details 1) organism, 2) sample size, 3) how significant is the CNV loss, 4) how big is the region of CNV loss, 5) how did you identify CNV loss, 6) how did you assess whether the gene expression was less, 7) how much less was the gene expression. All of these are important if you want a good answer. Thanks.

Yes, I think we need to look into chromatin states as well. Thank you for the link and the pointer to the previous question.

@user438383
I can answer some of these questions but I am not sure we can resolve this because these are computational results. I was looking at the underlying biology.

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When forming an enzyme-substrate complex in a spontaneous reaction, why does free energy increase?

We eat food and which is digested into proteins and carbohydrates.
Does digestion break bonds within food macro molecules and decreases free energy? Why, when looking at curve, do we see an increase in the free energy and then a decrease?

This increase is the activation energy: https://en.wikipedia.org/wiki/Activation_energy

Kinetics and thermodynamics are two separate things. The type of diagram you show is often encountered (even in textbooks) because it is thought to be a convenient hand-weaving way to convey a feeling of what is happening. However it is not correct as it mixes two different views: the microscopic molecular view (horizontal axis) and the macroscopic thermodynamic view (vertical axis).
The result is a misleading idea that the (molar?) Gibbs free energy (of what ???) can go up (event temporarily) along a spontaneous reaction. However for a spontaneous process (and "spontaneous" is key here) the Gibbs free energy of a system can never increase.
What can increase is the potential energy of a molecular system of the reacting molecules along a reaction path, which is what the vertical axis should represent. In which case the graph would represent a potential-energy profile. But defining a thermodynamic property like a molar Gibbs free energy for a single molecular entity has no meaning.
One might argue that considered as a chemical species, the transition state at the top of the curve (generally called the "activated complex") is obviously unstable and, considered collectively (i.e. macroscopically) must have a higher molar Gibbs free energy (at any specific time during the reaction). However, this is only partially true: it has a higher molar Gibbs free than the product towards which the flux of matter goes, but it necessarily has a lower molar Gibbs free energy than the reactants that are consumed (else the reactants would never form the said activated complex). Also, at the end of the reaction, when equilibrium is reached, all species have equal molar Gibbs free energy so that the Gibbs free energy of reaction is null ($\Delta_r G = 0$).
An alternative, really thermodynamic diagram is sometimes represented: the Gibbs energy diagram. In such diagram, the Gibbs energy of the successive species might appear to go up and down. But one should be careful of the impression given because such diagrams actually represent the standard Gibbs energies of the reactants, which is not their Gibbs free energy in any arbitrary state, and especially not necessarily their Gibbs free energy in the condition of the reaction considered.

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Advocate for the pop-culture idea of withholding vaccination
While it is widely accepted that vaccination is preferable to not vaccinating, would anyone like to give a shot at providing evidence in favor of not vaccinating? Anything goes.

This is a scientifically minded site. Why would you think we would want to engage in such a waste of time?

Here's the thing. No one has been able to repeat the results seen in the discredited "vaccination is linked to autism" study that started this whole dangerous mess (I'm not even going to bother looking up the citation, I care that little about it). Scientists, including those funded by so-called "anti-vax" groups, have been trying for the past 15-20ish years, and they can't do it, because
there is no causative link between early-childhood vaccination and autism.
Your question is akin to asking us to advocate against Pasteur's germ theory of disease, or for the idea of phlogiston in chemistry, or against the theory of relativity in physics.
So, given that the scientific evidence is firmly pointing in one direction, why would we waste our time on this endeavor, especially when anti-vaxxers will cling to any sort of misquoted, out-of-context, partial evidence that they can find?
The only reason a child should not receive a vaccine at the scheduled time and in the recommended dose would be because she is severely allergic to one of the main components of the vaccine, or she has a significantly-depressed immune system, typically associated with cancer and other severe medical conditions. At such times, medical recommendations by the specialist treating the condition should be followed.

Really good answer, however I don't want to vote up, because then the question will hang around even if closed. Maybe it should become a community wiki on why early childhood vaccination? Or an ask and answer? I'd vote up.

@AMR I wrote it out of frustration and because I didn't want to take 4 comments to say the same thing, not for upvotes :) The question can still be (manually) deleted after closure if enough 10K+ users vote to, so get your lobbying skills to work!

This has been covered already on Skeptics and Health, so I don't see the need to cover it again here.

Not to mention that "study" wasn't even a study at all. It was "hey, I looked at the guts of 6 of my patients and now I am convinced vaccines cause autism". What the heck? It's been retracted and denounced by the journal that published it by now, anyway.

Phlogiston! :'D

@DonJulian and why is that? Because we rigorously tested a hypothesis, found it to have no support, and discarded it? That's exactly what science is supposed to do.

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what is the natural way of rose to propagate by its vegetative cells?
I have read that rose reproduces sexually. But I have also heard that it can propagate by its vegetative cells (vegetative cells in its root). Is this correct? If yes, can I know how does it propagate by its roots?

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Wheatgrass in thalassaemia
In local newspapers there was a not so recent story about wheatgrass juice being "curative" in thalassaemia. Although I do not take the article at face value, it would be enlightening to know if there was any basis at all in the claims that wheatgrass juice or extract can help mitigate some symptoms of thalassaemia.

Wheatgrass juice or extract has shown some promise for reducing the required frequency of blood transfusions in thalassemic patients, possibly due to iron chelating activity.  However, few high-quality controlled studies have been conducted so it may be too early to form a definite conclusion.
References:

Choudhary, Dharma R.; Naithani, Rahul; Panigrahi, Inusha; Kumar, Rajat; Mahapatra, Manoranjan; Pati, Hara Prasad; Saxena, Renu; Choudhry, Ved P. (April 2009). "Effect of wheat grass therapy on transfusion requirement in β-thalassemia major". The Indian Journal of Pediatrics 76 (4). pp. 375—376. doi:10.1007/s12098-009-0004-6.
Das, Priyabrata; Mukhopadhyay, Ashis; Mandal2, Suvra; Chandra Pal, Bikas; Mishra, Raghwendra; Mukherjee, Debarati; Mukhopadhyay, Soma; Basak, Jayasri; Kar, Manoj (2012). "In vitro studies of iron chelation activity of purified active ingredients extracted from Triticum aestivum Linn. (wheat grass)". European Journal of Medicinal Plants 2 (2). pp. 113—124. doi:10.9734/EJMP/2012/1059.
Marwaha, R.K.; Bansal, Deepak; Kaur, Siftinder; Trehan, Amita (July 2004). "Wheat grass juice reduces transfusion requirement in patients with thalassemia major: A pilot study". Indian Pediatrics 41. pp. 716—720.
Mukhopadhyay, S.; Basak, J.; Kar, M.; Mandal, S.; Mukhopadhyay, A. (2009). "The role of iron chelation activity of wheat grass juice in patients with myelodysplastic syndrome". Journal of Clinical Oncology (Meeting Abstracts) 27 (15S). p. 7012.
Singh, Karnail; Pannu, M. S.; Singh, Palwinder; Singh, Jaswinder (January 2010). "Effect of wheat grass tablets on the frequency of blood transfusions in thalassemia major". The Indian Journal of Pediatrics 77 (1): 90—91. doi:10.1007/s12098-010-0002-8.
Tirgar, P. R.; Desai, T. R. (September 2011). "Investigation into iron chelating activity of Triticum aestivum (wheat grass) in iron-dextran induce iron overload model of thalassemia". Journal of Pharmacy Research 4 (9). ISSN 0974-6943.


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Absorption of Topical Magnesium
Can Magnesium be absorbed through the skin? Some athletes believe that Homeopathic magnesium lotions can reduce muscle pain. I've tried this and it doesn't work nor can I see how it can.

Homeopathic magnesium lotions don't* contain magnesium, so it seems a little irrelevant whether or not magnesium can be absorbed through the skin. However, magnesium ions can definitely be absorbed through the skin. There's no reason why that should reduce muscle pain(especially because ions would disperse throughout the bloodstream etc etc), but magnesium can be absorbed through the skin fairly efficiently.
*Footnote: they do, but not on purpose. If correctly prepared they would contain zero atoms of magnesium(depending on what 'strength' they are), but that kind of purity is impossible.


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Oxygen supply in a trickling filter
I'm using a 300l/h trickling filter consisting of 4 round chambers in vertical alignment with 11cm diameter, 5cm height and 5cm distance for the trickling (100 to 500 holes per level) in a 15cm pipe. The top is open in order to allow air exchange. 2 chambers are filled with 2 to 4mm gravel, one with filter cotton and one with clay pipes. It is used for nitrification of aquarium water.
The filter is loud and I want to muffle it. I already figured out that laying 2 levels of microfiber towel on top of it helps. I also have the option to build a wooden enclosure.
What measures should I take in order to reduce the available oxygen for the nitrifying bacteria as few as possible? Could the exchange through the towels be sufficient? Should I use a special membrane in the enclosure? Does it make sense to connect an aquarium air pump to the inside of the filter?


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Why does eyebrow growth stop after it reaches a specific length?
When compared to hair that grows forever after we cut it, why do eyebrows stop growing? What genes measure current length of eyebrow to ensure it stops growing after a specific length?

no gene measures the length, all hair grows for a period of time then goes dormant, eyebrow hair just grows for a much shorter period of time and grows slower. even head hair stops growing after a few (2-7) years. https://en.wikipedia.org/wiki/Human_hair_growth for more detail on the genetics You can start here https://www.ncbi.nlm.nih.gov/pubmed/5173315

If we cut it in the middle and in the base, why it regrow to the same length after all. I mean If we cut it in the base then it's need more time to regrow than if we cut it in the middle. But how gene determined this?

short answer, It doesn't

An interesting question, but backwards.  Almost all hair seems to grow only to a certain length (or for a certain length of time), then stop.  Human head hair seems to be one of the few exceptions.  The only others I can think of are wool sheep and horse manes.  As for human head hair stopping growth after a time, why am I still paying to have it cut every couple of months?

Does this answer your question? Why does hair grow after trimming but remains at a constant length after a while?

My eyebrows used to be 1 cm, and after 35 they could easily get to 6 cm, they grow for a specific time and are renewed.

@jamesqf - Stop getting it cut and see if it grows indefinitely. Some kinds of sheep will grow wool until it kills them if not shorn.

@anongoodnurse: I've actually tried that :-)  But I have very fine hair (oops, ambiguious language there, I mean the individual hairs are much thinner than most people's) so it only grows to about shoulder length before the hairs break. Especially considering that everything that sticks out from under a motorcycle helmet gets seriously windblown.  OTOH, I have one or two hairs in each eyebrow that seem to grow indefinitely...

@jamesqf - "I have one or two hairs in each eyebrow that seem to grow indefinitely..." Lol! Ok, you won that one! My hair, when young, made it down to my upper thighs, then stopped. Apparently my follicles had a long growth cycle. Decades later, it stops between my shoulder blades. Strange. Maybe my follicles are tired. :)

Activation of the mammalian gene Lhx2 leads to increased hair growth. Lhx2 is a transcription factor which regulates hair formation.

"...length of the hair is determined by the duration of the growth phase; for example, the growth phase for scalp hair can proceed for a number of years, while the growth phase for eyebrows last a few months."

Other genes that have been associated with hair disorders include: FOXN1, ALX4, HOXC13, MBTPS2, VDR, CDH3, HR and ANTXR.

I'm afraid I don't understand this answer.  People who shave their eyebrows regrow them (over a few months).  But your answer suggests that after an eyebrow hair begins its life, it grows for a few months, and then never ever grows again.  Or the eyebrow hair will once again re-start growth once it has been shaved?  How would the hair root know if the hair was cut?

@cowlinator - When I was a brand new doc, it was customary to shave either side of a laceration that went through the eyebrow before suturing it. But very soon after, the procedure changed, because 1. the rate of infection was no different between shaved and unshaved repairs, and 2. in some people, the shaved eyebrows never grew back. Can't tell you why, though.


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Do sieve tube cells have any extrachromosomal circular DNA at maturity?
In order to generate a tube system of low resistance, sieve elements lose most of their cellular components such as the nucleus, cytoskeleton, ribosomes, tonoplast etc.
Mature sieve elements contain structural phloem specific proteins (P-proteins), mitochondria, ER, and sieve elements plastids.
In plants, sieve tube cells lose their nuclei at maturity (just like our RBCs), and thus lose their chromosomal DNA, but they don't lose their mitochondria.
In eukaryotic cells Wikipedia has divided extrachromosomal DNA into three parts based on where it is seen (I guess):

Mitochondrial
Chloroplast
Circular

Sieve tube cells have mitochondrial extrachromosomal DNA at maturity, but I'm not sure about the existence of extrachromosomal circular DNA in these circumstances.
Do sieve tube cells have any extrachromosomal circular DNA at maturity?

Hey, got it wrong way around! Sieve cells lose the nucleus, not the companion cells.

@PolypipeWrangler Corrected! Sorry. I hadn't slept for nearly twenty-four hours when I was writing this question.

I can't add anything because the "edit" link under my question disappeared but this question is relevant.

This ref. says that the plastids and mitochondria are still intact.
Found by searching for "sieve cell development"
Neuberger, D.S., Evert, R.F. Structure and development of sieve cells in the primary phloem ofPinus resinosa . Protoplasma 87, 27–37 (1976). https://doi.org/10.1007/BF01623956
https://link.springer.com/article/10.1007/BF01623956

I can't add anything because the "edit" link under my question disappeared but this question is relevant.

I cannot edit either.

Mods should do something about it. Do you know an alive plant cell that has no nucleus and no other DNA simultaneously?

I dont know of any, apart from developing xylem cells.

You know I've seen a false/true question: An alive plant cell may have no organelles.

Maybe these developing xylem cells are intended by the questioner I don't know.


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View and plane/section of neural tube
I have a question regarding the following image:

In my book, it states that this is a dorsal view which shows the formation of the neural tube. However, isn't this a caudal view of a transverse section? A dorsal and ventral view wouldn't apply to a transverse section right?

It looks like a dorsal view to me, like your book says.
It isn't a section at all, these are embryonic structures visible from the outside.
Maybe you are being misled by the orientation of the neuraxis differing among organisms? The head will develop at the anterior neuropore; the spine will develop down the middle. You are looking at what will be the back.
Here's another view from Gray's (downloaded from Wikipedia at https://en.wikipedia.org/wiki/Somite#/media/File:Gray20.png ):

Thank you for your answer. The neural folding was shown from two different perspectives. The first perspective being the original image in the post and the second one being: https://i0.wp.com/veteriankey.com/wp-content/uploads/2017/09/c16f002-1.gif?w=960
That image is a 'sagittal section'. In that case, isn't the original image the top (cranial) view of this section?

@Stallmp It doesn't make much sense to refer to a "cranial" view when there is no cranium. Certainly neither of these is a sagittal section, though. Your second image in the comment is a transverse slice; in that image, dorsal is "up". Can you provide a citation from what book this is or at least a more complete image? You've cut off all the description and explanation.

So if you look at the original post in my message, this is apparently a dorsal view as mentioned. There is also an anterior neuropore, which is the cranial neuropore, and a posterior neuropore, which is the caudal neuropore. In that case, isn't the second image a 'sagittal' view of either the cranial or caudal neuropore?

No, the second image is not a sagittal view of anything, and it is not showing a neuropore. In (B), you see the neural folds closing in, such that in (C) it has closed and formed a neural canal. So it's from someplace in the middle of the first image. See the "somites" on each image (same thing as "primitive segments" on the one I posted)?


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What are Palomena prasina doing in my home?
I live in eastern Europe, and every autumn, ever so often a Palomena prasina flies inside my home.
I have an avocado plant that I put them on to live - I currently have 5 of these on my plant
However, I have noticed they hardly if ever eat the plant and they hardly if ever move, and I haven't noticed poo either (they are alive). I was thinking that they are waiting the winter to pass and kind of hibernate, but if this is the case, firstly - how can they tell, and secondly - isn't their lifespan too short to wait for the spring?

Many people call many different things 'stink bugs.' You will have to be more precise with what bug you are referring to (species ideally, genus is probably okay). I don't know if they can be "hibernating" (overwintering) on your indoor plant - is your indoor avocado plant kept at room temperature?

I believe it is Palomena prasina


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Why do neurons lose the potential to regenerate and reproduce in adult animals?
I have read in several books that neurons in the central nervous system lose the power to regenerate after some developmental stage but why do they? Can we artificially induce regeneration?

There's roadblocks to stop nerve regeneration, perhaps the organization of the brain means that making new brain cells would re-wire you and make you confused. Most vertebrates that have a damaged spine or brain would be dead anyway, given the force required to damage a fish or a lizard spine, it's not that useful for vertebrates, it's in the most protected, tough, defended zone of the animal, so structurally the animal wouldnt have the time to heal for food and drink and defense while the nerves also mend themselves. afterwards the knee and hip nerves might have swapped round left and right.

Neurons do not regenerate! If we could regenerate neurons, we would be able to help paralyzed patients regain their movement and help people with dementia and Alzheimers regain their memory and cognition. Neurons can regenerate axons if the cell body (soma) is intact, but otherwise, they cannot. There is more info on this site, and a few things on wikipedia as well. https://askabiologist.asu.edu/regeneration Hope this helps!

To answer the first part of your question: In order to regenerate, the neurons need to divide. In order to do that they need to round up so that they can form a mitotic spindle that sorts the chromosomes and makes sure that each daughter cell gets exactly one copy of the genome. For most animal cells this genome sorting only works in rounded cells, which is why neurons need to round up before they divide.
However for a Neuron, rounding up would mean that the neuron needs to retract its axon as well as all its dendrites. To do so is physically impossible for most neurons simply because of the length and complexity of the axon and dendrites (the axons of human motor neurons can be more than a meter long). See also the image below.

Even if retracting the axon and dendrite network was possible, this would mean that the neuron would lose its function completely because it would lose all connections to other neurons and with them all information it has stored. Thus, from an evolutionary standpoint it does not make sense to regenerate a neuron once it has matured and started to form connections with other neurons.
That being said, despite the fact that matured neurons cannot divide any more, our brain and our nervous system retain a lot of regenerative potential:

Provided that there is little scarring at the wound, a nerve fiber (consisting mainly of axons of neurons) can regrow because the neurons don't necessarily die when their axon is cut and they can regrow a new axon. The main difficulty for regeneration in this case is for the axon to find the path to its destination. Therefore it is important that there is minimal scar tissue (glial scar) because scar tissue prevents regrowing axons from finding their path.
The brain retains some neural progenitor (stem) cells that are able to differentiate into new neurons even at old age (but not as many stem cells as other tissue).
When parts of the brain are damaged, other regions can often take over that functionality (for example by by rewiring their axons and dendrites) a process called neuroplasticity. For example, people can often re-learn to speak after a stroke.

As to the second question: Using stem cell technology it is possible to grow fresh neurons in cell culture. In principle, these neurons (or rather their progenitor cells that mature into neurons) can be implanted in order to regenerate nervous tissue in the central nervous system. However, this cannot solve the problem that once the neurons are dead, even a new neuron that replaces the dead one cannot recreate all the connections that the old one had.
Replacing neurons is like replacing the hard disk of a computer. All information is lost. Therefore, current research on the therapy of spinal chord injury focuses on the prevention of scarring in order to help the existing neurons to regrow the axons and reconnect the body with the brain.
Edit: added references.


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Explanation for the results of Topoisomerase I treatment of ERCs - Gel Electrophoresis
This part of a 1997 paper published in The Cell (David A. Sinclair & Leonard Guarente, 1997) discusses the presence of extrachromosomal rDNA circles (ERCs) in greater numbers in old mutant yeast cells when compared to young ones. All the lanes to the right of the "old untreated" lane are treatments carried out to the old yeast cells.
There are two scales on the figure, the left hand side has a scale for the length of linear DNA, while the right has one for circular DNA (I think?) which appears to move faster through the gel than linear DNA of an equivalent size.
Excluding the Kpn1 lanes and the young yeast cell lane, there are two clusters of bands around 19.3kb ccc and just above 40.4kb ccc. Would I be right in thinking that the writers are saying these clusters are due to the presence of concatenated ERCs (near the 40.4kb ccc marker) and non-concatenated ERCs (near the 19.3kb ccc marker)?
I don't understand the results of the topoisomerase I treatment, it doesn't look to change the gel much when compared to the old untreated yeast lane. The description states that the topoisomerase I treated rDNA migrates more slowly through the gel, though this doesn't seem evident from the figure. There is a "linear genomic [rDNA]" label on the LHS above the 40kb ccc on the RHS, though I am unsure what it is referring to. Presumably it is the size of fragments of the genomic rDNA after it has been treated with another restriction enzyme? But there is no prior restriction enzyme treatment mentioned. This is the part I am least sure about.
Excerpt from the paper relating to the figure in question is below, and the full paper is linked here.

Several experiments were performed to investigate whether the circular rDNA molecules were oligomers of the 9.1 kb rDNA repeat. The
rDNA molecules had a faster mobility relative to linear DNA size
standards in the absence of ethidium bromide, a known property of
circular DNA (Figure 3, between the 19.3 and 40.4 kb size markers).
Digestion of old genomic DNA with KpnI (which cleaves once within the
rDNA repeat unit) prior to electrophoresis reduced the ladder of bands
to a single 9.1 kb species, demonstrating that the circular rDNA
molecules consist of directly repeated multiples of the rDNA unit
(Figure 3). Further, cleavage with BamHI had no effect on the banding
pattern since rDNA is refractory to this enzyme. A partial KpnI digest
reduced the abundance of the large circular species, while increasing
the abundance of smaller ones. This implies that the large species are
comprised of interlocked smaller circles (i.e., concatamers) that are
released during digestion. Finally, treatment of the DNA with
topoisomerase I, an enzyme known to relax supercoiled DNA, caused the
mobility of these DNA species to migrate more slowly, coincident with
the linear genomic rDNA (Figure 3). By quantitating the levels of
total linear and extrachromosomal DNA from old wild-type cells (see
Experimental Procedures), we estimate that the amount of ERC DNA in
old cells can reach levels equal to the total linear yeast genome.

Thank you for your help.

I’m voting to close this question because this site exists to answer specific problems in biology that are likely to be of general interest. It is not a journal club to discuss the details of particular published papers.

I think it's okay to ask about particular papers, but some problems about this post are that the title is not a question or suggestive of a question, and the apparent question asked here is buried deep in the body of the post.

Thanks for your help! have changed the title and the length of the post. Just wanted to provide some context without people having to comb through the paper.


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How does embryology provide evidence for evolution?
I am not a biology student, I just have a profound fascination and appreciation for biology, and from time to time I like to read and watch videos about it.
I was reading about evolution when I came across different evidence in favor of it, like genealogy, fossil records and embryology. However, it isn't quite clear to me as how embryology provides evidence for evolution.
The way I understand is this - and please correct me, if I am wrong here, - when we observe fetuses of different species, we observe some similarities in the development of those fetuses. But what I am not clear about is how exactly these similarities tell us that through the process of genetic mutation, we obtain new species. What am I missing here? I understand how genetic similarities tell us that we have a common ancestor, and how fossil records show the same.
If you can explain this to me, in words that a layman would understand, then I would be very very thankful. I would also like to know other lines of evidences for evolution in somewhat detail then that would be amazing.

I think you're forgetting that evolution means common ancestors in addition to mutation and natural selection.

Similarities of development between species can be interpreted in a roughly similar fashion as similarities of nucleotide sequence. I am confused why you think that a similarity of development could tell you "that through the process of genetic mutation, we obtain new species". Speciation and evolution are rather more than that! I would suggest reading about the field a bit, here is one review paper.

There's an old and mostly discarded notion that “ontogeny recapitulates phylogeny”, and I think that's what you're expressing here. Just forget about it.

This might interest you

See phylotypic stage.

Srinidhi, the video in the above link explains the idea of embryo development and evolution, Did you find it helpful? It's expressed in layman's terms.

When observing fetuses of different species, some similarities in the development of those fetuses are observed.
These similarities suggest that they may share common genes.
Conversely, differences suggest that they may have become a new species through a process of mutation.
Of course, they need to be investigated in detail genetically to see if they are not the result of convergent evolution or adaptive divergence.


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Why is $H_{S}$ divided by $H_{T}$ in Wright's $F_{st}$ equation?
$F_{st} = H_{t}-\frac{H_{s}}{H_{T}}$, where $H_{T}$ stands for expected average heterozygosity in the meta population and $H_{S}$ stands for expected average heterozygosity in the sub-population.
As I understand it, $H_{T}$ is the heterozygosity assuming that all of the sub-populations are from the same population and if it's true, there would be no gap with $H_{S}$ (if it's in Hardy-Weinberg equilibrium).
Than why is it divided again with $H_{T}$? Is it some kind of standardisation? I don't think it's necessary.
Why can't it be used like heterozygosity of population of meta population (variation of meta population)/heterozygosity of sub populations (variation of sub-populations) somewhat like F-value of F-test.
Also why is it done with expected heterozygosity, not with observed heterozygosity
I'm talking about fixation index and as I know, there are some other formulas for fixation index but this one is commonly used
uwyo.edu/dbmcd/popecol/maylects/fst.html

There are multiple distinct statistics called "Fst". What are you referring to specifically?

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

I'm talking about fixation index and as I know, there are some other formulas for fixation index but this one is commonly used
http://www.uwyo.edu/dbmcd/popecol/maylects/fst.html

$F_{ST}$, as defined by Nei 1973, is $F_{ST} = \frac{H_T-H_S}{H_T}$ and not $F_{ST} = H_T -  \frac{H_S}{H_T}$. It is, to my knowledge, equivalent to to original Wright's definition $F_{ST} = \frac{var(p)}{\bar p}$, where $var(p)$ is the mean (over all loci) variance (over all subpopulations) in allele frequency and $\bar p$ is the mean (over all loci) mean (over all subpopulations) allele frequency. Other formulations exist, either considering population weights or considering specific bias in estimate (e.g. Weir-Cockerham)


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How does the total number of genes increase throughout the course of evolution?
Campbell Biology says:

A typical prokaryotic cell has  about 3,000 genes in its DNA, while a
human cell has about  21,300 genes.

If evolution depends on random mutations occurring in the genome, this means that only certain genes are altered, but not add up to the total number. Supposing that we and the bacteria come from a common ancestor, then what is responsible for the tremendous amount of genes that has been added throughout the evolution?

"If evolution depends on the random mutations occurring in the genome, this means that we only alter certain genes, but not add up to the total number" - Why? Are you thinking only of point mutations? Also note that bacteria and humans have been evolving for the same length of time, and bacteria have had far, far more generations to evolve than humans have.

"Are you thinking only of point mutations?" - This is the case, mutations are the only thing I can think of right now. Can you point out other factors?

I didn't say "mutation", I said "point mutation". You may even only be thinking of specifically substitution mutations. You could start with https://en.wikipedia.org/wiki/Mutation to learn about others.

Look up gene duplications, copy number variations and transposons. That may give you a clue.

For a less mechanistic and more theoretical view, I would suggest looking into the evolution of complexity (that's just one ref it's a large literature). Obviously expanding to a view of mutation beyond substitutions is essential, as suggested by other commenters.

It's possible that interspecies hybridization resulting in temporary allopolyploids is a driver in this. There's some interesting material on carp, I'd recommend reading.


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Trying to identify a mushroom found in my backyard
I'm new at trying to describe mushrooms though I will try my best.

subtract from growth : grass
color : light grey/brown then a faded orange at the top
gill color is also light brown
ovate shape
believe the gills attachment is adnate
I think that this mushroom could be part of the coprinopsis family and found that the coprinopsis martini is pretty similar
-Also could possibly be a humpback inkcap
location is southern Georgia (USA)
extremely delicate, it ripped very easily

Were they growing in open area or in shade? Where they growing in a circular pattern or randomly? Over a wide area or clustered together?

From my experience, this is definitely a species of Coprinopsis, as you said. However, when it comes to this and related genera I find that the great diversity of species makes it pretty hard to pin down IDs. Coprinopsis martinii/acuminata like you suggested indeed seem pretty promising appearance-wise, but like I said you'll find this to be the case with many species of this genus, and neither seem very biogeographically relevant to Georgia. Try using iNaturalist to search the area for Coprinopsis species and narrow down your search from there.


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Problem: What is this pattern of inheritance?
The following question was on a pretest of mine, and I'm trying to figure out the answer using what we've learned about Mendelian and non-Mendelian patterns of inheritance. I'm struggling quite a lot with this question; I'm not sure if that's because of me or if the question itself is poor/confusing.
I don't know what the answer actually is, as there was no answer key to go along with the exam. My best guess is that the pattern of inheritance is Incomplete Dominance based on the Red x Yellow cross and the fact that neither allele was dominant over the other in the resulting progeny. But is it even possible to state this with full confidence? What about the other crosses?

In a plant species, plants may produce red, yellow, or orange flowers. The table below shows the results of crosses between the plants that produce each flower color.

Based on this information, which pattern of inheritance controls flower color in this plant species?
(A) Codominance
(B) Complete dominance
(C) Incomplete dominance
(D) Multiple alleles

The answer is incomplete dominance.
It can't be codominance, because codiminance involves both phenotypes being expressed in different parts of the organism: you would end up with red and yellow spotted flowers.
It obviously isn't complete dominance, because the red x yellow cross produces orange flowers.
Knowing that it has to be incomplete dominance or multiple alleles, we can examine what we would expect to see in either of these cases.
Multiple alleles
In the case of multiple alleles, each individual plant has two alleles out of a possible three. These alleles will also express some sort of dominance pattern over each other. Let's say, hypothetically, that the dominance pattern goes Red > Orange > Yellow.
In this case, all of the yellow flowers would have a genotype of yellow/yellow. The orange flowers could be orange/yellow or orange/orange. Red flowers can be red/orange, red/yellow, or red/red. When performing the crosses between red and yellow, you would then expect some mixture of offspring, probably mostly red. If the dominance pattern was different, you would still expect to see some mixture of offspring. But instead we see only orange offspring.
Incomplete dominance
In this scenario, homozygote red individuals have a red phenotype, homozygote yellow individuals have a yellow phenotype, and heterozygous individuals have the mixed orange phenotype.
In this scenario, you would expect red x red to produce only red offspring, and the same goes for yellow x yellow, because both parents have to be homozygous. Orange x orange would produce offspring in a genotype ratio of 1:2:1, as is the case when you self-cross heterozygous organisms. Orange x red and orange x yellow will produce offspring in a 1:1 genotype ratio, as is the case when you cross a heterozygote with a homozygote. These are exactly the patterns we see, so we can conclude that the answer is incomplete dominance.

Thanks so much for your thorough response, this question was bothering me. But I see how one would arrive at that answer now.

Are you saying that for the answer to be multiple alleles, each phenotype needs to be represented my an allele? So one Red, one Orange, and one Yellow? Is that the technical definition of multiple alleles for inheritance? It seems like that is a bit of a confusing answer choice, as there have to be different alleles for red and yellow, at a minimum.

@AMR Yes, that's the definition I'm using. I guess the wording is a bit confusing

@CactusWoman But according to my textbook, "multiple allele" refers to inheritance involving a single gene that has 3 or more alleles, such as the gene that codes for blood type (which has alleles I^A, I^B, and i). What would be the difference between, say, blood type and the flowers in this case?

@AleksandrH That is what we are saying. In your flower example multiple allele would mean there is a Red allele, an Orange allele, and a Yellow allele, however, in the example of the questions, there is no Orange Allele. A Red/Yellow Heterozygous will have an Orange phenotype, but there is no actual Orange allele, only an Orange phenotype.

Ah, I see what you guys mean now. So the fact that a Red + Yellow cross can produce Orange implies that there is no "orange" allele, correct? Rather, the orange flowers are produced as a result of incomplete dominance between the Red and Yellow alleles?

@AleksandrH Correct, the orange phenotype is the result of the heterozygous red/yellow genotype.


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Measuring Gross Primary Productivity (GPP) using Light and Dark Bottle methods: Sample Question
The following question is taken from my Cliffnotes AP Biology 4th edition practice exam and it deals with the light and dark method for measuring gross primary productivity.

In a classroom investigation, students filled two bottles with pond water containing only photosynthesizing organisms. They used a dissolved oxygen (DO2) sensor to measure the amount of dissolved oxygen in each bottle. One bottle was put under a light. The second bottle was wrapped with aluminum foil to block all light and was put under the same light. AFter 24 hours, pond water DO2 in the two bottles was again measured. Average values for DO2 from all students are provided in the following table.

Calculate the gross primary productivity for the observed sample. Express your answer in mg fixed carbon/L/day to the nearest hundredth.

Okay, so I know that net primary production (NPP) is the difference between gross primary production (from photosynthesis) minus Autotrophic respiration (Ra):
NPP = GPP - Ra
I also understand that the light bottle is measuring NPP, because it allows for both photosynthesis and cellular respiration. The dark bottle measures Ra because it only allows for respiration. Therefore, GPP can be calculated by rearranging the formula:
GPP = NPP + Ra
Calculating the difference in the final and initial values for both bottles, I get the following:

Light: 0.15 mg O2 / L   <-- NPP
Dark: -0.08 mg O2 / L   <-- Ra

Next, I plugged these into the formula:

GPP = 0.15 - 0.08 = 0.07 mg O2 / L

Using the conversion formulas provided on the College Board's AP Bio Appendix (essentially just multiplying the mg O2 / L value by 0.374128 to get mg Carbon fixed / L), I get the following:

0.07 mg O2 / L * 0.374128 = 0.02618896 mg C fixed / L

But according to my review book's solution, I was supposed to add 0.08, not subtract it. This seems a bit strange to me. Is this a mistake in the book or am I not understanding something?

The dynamics are:
Light bottle: GPP - Ra = 0.15
Dark bottle : Ra = 0.08

Then GPP = 0.15 + 0.08.
The amount of O2 used in the respiration is 0.08 mg O2 / L, not -0.08 mg O2 / L.

If you think about what is going on in the light bottle, this should make more sense.  Oxygen is being produced by photosynthesis, but respiration is using up the oxygen being produced.  Therefore, the total amount is NPP.  So if you want to find out how much oxygen was originally created through photosynthesis (GPP), you need to put those losses due to cellular respiration back into the light bottle (in other words, add the R amount to the light bottle amount).

Your wish to help the poster is admirable, but as you are a new user, may I suggest you check the dates of questions. This one was posted in 2016, so I imagine the poster has moved on to other things. You may wonder why it has resurfaced after three years. This happens when a question hasn’t had an answer with enough votes to be “put to bed”, and the reposting is to give people an opportunity to review and vote for the answers.  (Unlikely for this sort of homework question.)

I have moved on to other things! But it's okay, lol.


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What is the difference between a macrophage and dendritic cell?
I am aware that both these cells (monocytes) are phagocytes and are able to present antigens upon their own Class II - MHC integral proteins.
Other than their difference in structure (size and shape), what other differences do they have? For example, do they engage with T-Cells differently?

Macrophages can only activate the general T - Cells while dendritic cells can activate memory T - cells as well. Also, dendritic cells don't survive after their effector function while macrophages do. The main difference is the fact that dendritic cells present pathogens to T-cells while macrophages initiate the main response of removing the pathogen and then presenting their peptides to other cells.
This link might be helpful as well.

Hi Shadan. Thanks for answering. To improve your answer, please include credible references to support specific statements, otherwise the answer to such a rather specific question is suspect and will be downvoted. Scientifically, using phrases like "from what I know" and "I would say..." are unfortunately worse than unhelpful, they cast doubt or confusion, and take away from the link that you share at the end, which you may have quoted to answer the question very elegantly!


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Human gene number distribution on different strands of the chromosomes
I cannot find an article that describes the gene distribution based on their appearances on different strands and if I find one, like this from 2007, there are some aspects which are confusing, for instance:

A total of 12,692 loci were present on the positive strand, with
12,442 on the negative strand.

How are positive and negative strands determined in general if we are not talking about a particular gene at a particular locus?
Aren't both strands similar in a way that we can not name one as a sense, antisense, template, or coding? Are not both strands in a chromosome used for transcription in a symmetric way?
Any article related to my main question (in the headline) or explanation about this confusion in this article would help.

For humans and other eukaryotes, the convention is that the "start" of each chromosome is the end closest to the centromere:

In all human reference chromosomes, as for other eukaryotes [3], the plus (+) strand is defined as the strand with its 5′ end at the tip of the short arm [4,5] (Genome Reference Consortium, personal communication, March 27, 2012).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6099125/


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Which statistical test should be used for GC-content comparison?
I'm predicting that certain genes (n=20) are more GC rich than expected in all protein-coding genes. How can I test this hypothesis efficiently?
I generated the same number of random genes (also n=20) and calculated GC content for them. After using the t-test (2-tailed, two-sample unequal variance) it shows a significant P < 0.005 result. But I'm not sure that I can interpret it with high confidence.

Crossposted https://www.biostars.org/p/9525660/

You could try a permutation test. These are a kind of non-parametric statistical test which involve creating your own null distribution from your data.
Your hypothesis $H_{1}$ in this case, is that your gene set has a higher GC content than expected by chance. Similarly, your null hypothesis, $H_{0}$ is that there is there is no difference between your set a random set of gene from the population. You are interested in a p-value, which simply asks what the probability of obtaining  a test result at least as extreme as the result actually observed, under the assumption that the null hypothesis is correct.
So thus to obtain a p-value and take say, 1000 random samples of protein-coding genes and calculate their GC content to obtain a null distribution. Then to obtain a p-value that your gene set has a higher GC content than expected under the null, take the proportion of the null distribution greater than your gene set.

I feel you should be comparing your 20 genes against all other protein coding genes in the same organism.
A statistical test comparing the proportion of GC nucleotides in your sample to the rest may be the one to use.


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Superbugs in eusocial animals
I am not a biologist, and I'm interested in eusocial animals, and the porous habitats in which they live. I know few facts about diseases in these animals: I know some interesting instances of viruses, bugs and about cancer, respectively [1] in Spanish, the hygroscopic property of honey (I don't know the article [2]), and [3].
Question. I would like to know if there are eusocial animals which suffer diseases due to superbugs. In such case add the most relevant facts from your knowledges or cite/refer the most relevant articles from the literature.
I add as general references that Wikipedia have edited the article Eusociality and Antimicrobial resistance redirected from the search Superbug (https://en.wikipedia.org/wiki/Super_Bug). I hope that my question does make sense (for some eusocial species), in other case I can to delete my post. Feel free to add your feedback in comments if my post isn't suitable for your site Biology Stack Exchange.
References:
[1] David Pride, Los virus de nuestro cuerpo, Investigación y Ciencia, Febrero 2021, Nº 533, pages. 76-83.
[2] Manisha Deb Mandal and Shyamapada Mandal, Honey: its medicinal property and antibacterial activity, Asian Pac J Trop Biomed. 2011 Apr; 1(2): pages 154–160.
[3] Elizabeth Pennisi, Why Naked Mole Rats Don't Get Cancer, from the web of Science (19 Jun 2013).

Welcome to the site. Please take a [tour] and visit the [help] for more information on what we do here and what makes a good question and answer. In particular, have a look at the homework section and see how that applies to your question. As it stands there is little linking your statement in para 1 to the question and the references to cancer and honey don't seem appropriate given that these have nothing to do with superbugs.

If I understand right, you are considering the antibacterial properties of honey to be similar to antibiotics, considering other eusocial animals may produce anti-pathogen substances, and asking if pathogens that resist these substances cause disease in the eusocial animals. Is that correct?

No, I don't assert it, and I'm sorry @timeskull if I've introduced a misunderstanding with my references. The references cited [1], [2] are to illustrate that I know that some eusocial animals suffer infections/ diseases caused (respectively) by viruses and bacteria, and that the case of cancer was studied in the mammals in [3]. I would like to know if there is some eusocial animals that suffer disesas causes by superbugs. Many thanks and I hope don't bother you or your colleagues (professors of the site).

Well, a "superbug" is a pathogen that is resistant to antibiotics or antifungals. No eusocial animals produce those so resistance wouldn't affect them.

Not an answer because I can't give a definitive yes/no to eusocial animals. Well, human to dog transfer of MRSA has been recorded in 2004, and although dogs/wolves are not technically eusocial, it would indicate a first step in the transmission to non-human animals. Superbugs in livestock are a matter of great concern too.

Many thanks for the comments @JiminyCricket. and for your colleagues


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Arguments against incest
Incest is forbidden in most countries because if there is a genetic disease in the family the child of a incestuous relationship will be at least holder of the gene of that disease. But lets say the members of a family dont  have a genetic disease and are not holders of any gene related to a genetic disease then theoretically would a child of a incestuous relationship not suffer from diseases by birth?

@JiminyCricket. Editted.There are dominant genes and less dominant genes for every trait of a human person for example lets say for the color of the eyes if someone inherits the gene which translates to the brown eyes from his dad and the gene which translates to the blue eyes from his mum then because the gene which translates to the brown eyes is more dominant than the gene which translates to the blue eyes , the kid will be born with having brown color eyes,yet he will be a holder or a carrier of the gene for blue eyes.

evolution is about probability, the probability of your hypothetical assumption is breathtakingly low. That's why an avoidance instinct exists, not because it it always holds true.

There is more to it than just the biological risk, there's also morale issues and the fact humans developed a family structure. (That's better discussed on a different site, or in chat.)

Incest doesn't necessarily mean that the partners are having unprotected sexual intercourse. It simply means sexual intercourse between closely related member of a family. In case of protected sexual intercourse, it doesn't matter whether or not the family has history of some genetic disorder.
But let's say they are practicing unprotected sexual intercourse. In that case, it does depend on the genetic history of the family. If either or both of the parthers has gene that result in a disorder, then thier offspring who gets that gene expressed in his/her body will suffer from that genetic disorder. And if it is not expressed, they become a carrier for that gene.
Now, coming to the case you mentioned, Yes, if neither of the partner have gene that causes certain genetic disorder, then the offspring will not suffer from the said gentic disorder.
But it only works if there's a no history of incest wihtin that family. In case they do have history of incest within thier family, they are likely to suffer from inbreeding depression. Inbreeding depression 'exposes' deleterious recessive genes by making them homozygous. This causes drop in fitness of the offspring and reduced fertility. Increased homozygosity is what causes issue, which increases chances of a harmful recessive gene getting expressed.
So it's not a big worry, if they don't have any such gene that cause obvious harm by resulting in a certain genetic disorder. But continuous incest in family may result in problems later on.
Anyway, it is possible to be able to determine compatibility of two people by checking thier genetic information [we may become even more advance in near future]. We can selectively edit a gene to make it so that it won't be present in the offspring. Gene editing at advance level will get really popular.


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Maximum Allometry of aquatic mammals omitting Kleiber's Law
As far as I understand, blue whales cannot get any physically larger due to the extremely demanding caloric intake it has on consuming large quantities of krill, not due to any other physiological reasons, as it for what limits a land animals's, being their bones not being able to support their own weight.
Be that the case, how big can an aquatic mammal be, in terms of volume and/or mass?
Would other organism's, such as Hydrozoa, to name one example, display any difference in this regard?
For reference on the Blue Whale size being limited by caloric consumption, here is a link on a study:
https://science.sciencemag.org/content/366/6471/1367.abstract
Goldbogen, J. A., et al. "Why whales are big but not bigger: Physiological drivers and ecological limits in the age of ocean giants." Science 366.6471 (2019): 1367-1372.
APA

Welcome to the site! "As far as I understand" is really insufficient... please source your claim, and demonstrate what research you have done so far.  Thanks!

Thank you! Yes, I will post a link to what I am referencing about.
I am not studying biology as my main career, that being Material Science, but I have always have had a fascination with marine biology, so pardon if sometimes my knowledge isn’t up to standard.


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Asymmetric sequencing | Can you sequence 250 bases on Illumina Novaseq S4 (read 2)?
I would like to sequence 250 bases on Illumina Novaseq S4 on read 2.

Kits of illumina come in the following sizes: https://emea.illumina.com/systems/sequencing-platforms/novaseq/specifications.html

You can setup the sequencer for asymmetric sequencing, so that from a standard paired-end 2*100bp kit reads 150 bases from R1, and only 50 of the R2 (or vice versa).

On SP kit they now support 2 x 250 bp, but not on S4.

On the largest S4 kit it would be theoretically possible to sequence 250 + 50.

The read quality at 150 bases is excellent, so I expect at least 200 useful bases.

Did anyone try this, or could point me to relevant information?
Can you even specify such strong asymmetry in the software?
Very importantly: Are there any risk of losing the lane?
Are there any other risks (other than quality issues beyond 150 bases, which i assume I can easily trim away)?

ps.: Cross posted on seqanswers for a possibly more appropriate audience.

I have done this on MiSeq and NextSeq though it was several years now. It is possible to specify cycle numbers in the GUI input (page 54) in theory, unless they changed things (though they only mention up to 151 cycles).
I previously emailed Illumina technical support about this (the docs for the NextSeq also said "up to 151 cycles") and they said this:

The reason the MiSeq 300 cycle kit supports for 250x50 is because the MiSeq chemistry has been tested at those long run lengths and the same chemistry is implemented in the 500 cycle kit that allows for 2x250. In the case of the NextSeq, there is no 500 cycle kit and it has not been tested for run lengths beyond 151. That said, there should not be anything in the software that prevents you from running a 250x50 on a NextSeq 300 cycle kit, but the quality for any cycles past 150 may be low.

It might be worth following up with them to make sure that it would still work.
For our application, the quality was sufficiently good that we were able to use the data (from a capture panel). Admittedly, we were using a somewhat bespoke alignment strategy rather than e.g. traditional variant calling.

Thank you so mcu!  We also used asymmetry in other setups,  without problems, but at the end we went with standard settings here - it was too expensive to risk anything going wrong!


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Do photosynthesis and respiration violate the law of conservation of energy?
I don't know, if it's a physics question, biology or chemistry question but anyways here it is:
I have been taught that to produce one molecule of glucose in photosynthesis, 18 ATP molecules are used up, but that in respiration, oxidation of the same glucose molecule releases 38 ATP molecules. I just can't seem to wrap my head around it. Where are these extra 20 ATP molecules coming from (or in other words extra 20 units of energy)?
I know there's a whole lot of reactions occurring in the cell that utilize energy, but the reactions of photosynthesis and respiration are reversible and I don't think the path to make or break glucose actually matters with respect to the amount of energy used or released in the processes. Glucose always remains glucose so of course writing the same reactions in reverse orders shouldn't change the energy used/given out in the reaction.
I really can't understand why it should it depend on the path by which glucose is used or made as many people have told me.
So in my opinion these two processes do seem to violate the law of conservation of energy, so please help!

"Does X violate the law of conservation of energy?" -> No.

The same question with physics-minded answers: https://physics.stackexchange.com/q/707262/247642

@EricDuminil For X that actually happens, that is. It's very much a good sanity check for when you're developing a new hypothesis :D

As for "it should always give X amounts of energy regardless of 'the path'" -- not related to this question directly, but you'll find that aerobic vs. anaerobic can make a huge difference when trying to get energy out of molecules. ;-)

@EricDuminil It would be better if questions like this started with "Why doesn't" instead of "Do", because I suspect the OP doesn't actually wonder if it violates the law of CoE, but rather wants to be enlightened as to what is really happening.

With slight adjustments to the scientific wording, what the poster states is in effect:

“…to produce one molecule of glucose in photosynthesis, 18 ATP molecules are used up hydrolysed”

and

“…oxidation of the same a glucose molecule releases phosphoryates 38 ADP molecules to ATP”

These statements are both correct…
…but the logical fallacy arises because the first one is incomplete.
In the context of energy production and utilization, it is essential to add:

…and 12 molecules of NADPH are used (i.e. oxidized to NADP)

This is because 1 molecule of NADPH is energetically equivalent to 3 molecules of ATP.(Oxidative phosphorylation will convert NADPH + 3ADP to NADP+ + 3ATP).
Hence it takes 54 ATP equivalents to synthesize a molecule of glucose, but one only gets (approx) 38 molecules of ATP from oxidizing glucose.
If you think right back to the light reactions of photosynthesis, the photons of light energy are used to do two things — phosphorylate ADP to ATP, and to reduce NADP+ to NADPH.

Where are these extra 20 ATP molecules coming from (or in other words
extra 20 units of energy)?

The sun.  They are provided by high energy photons emitted by the sun.  Those photons excite electrons into being in a higher energy state, and that higher energy electron state is harnessed and changed into high energy chemical bonds, like in ATP.

The 18 ATP comes from the sun. The extra 20 ATP doesn't.

@mathlander but it does!


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Why does the thymus gland shrink with age?
What exactly is reason/process/mechanism for which our thymus gland starts to shrink with age? The thymus gland is the site of production of T lymphocytes which are the best defence against infection and even cancer cells, but as we mature, the tissue shrinks and gets replaced by nothing but fat.
Whereas our bone marrow (although it gets reduced cellularity) stays mostly intact and keeps producing red blood cells. I scoured the web for answers but didnt got satisfactory answer, with mostly dealing with effects rather than cause. One Quora answer draws speculation that perhaps with old age, thymus cells accumulate mutations so its better for body to reduce it, but it doesnt seems satisfactory.

@Kshtij Kumar. Intuitively, it must be supposed that 'thymic involution', a process mediated by circulating sex hormones (post-pubertally), occurs because its principal function as the site for maturation of T-lymphocytes has been largely satisfied once processes of their positive and negative selection have been accomplished. Since these T-cells are both long-lived and exposed to the circulation of blood and lymph, these 2 aspects of T-cell maturation are substantially complete in the thymus itself: its role is fulfilled. Incidentally, the original thymocytes are produced in the bone marrow.

If you read the 'Wikipedia' article on the 'thymus' carefully, the mechanisms are mentioned by which these long-lived T-cells are programmed in the thymus to recognise the difference between foreign antigens presented to their surface receptors by the MHC of body cells, and autoantigens deriving within the body itself -- i.e. 'positive selection' ('negative selection' of T-cells reacting to autoantigens results in apoptosis of the thymocyte within the thymic medulla). The inference is that once the bulk of this function is achieved in the thymus, refinement of the process occurs peripherally.


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Why do some viruses get deadlier over time?
I was wondering what reasons are that make some viruses become more lethal over time.
By "more lethal", I am not referring to acquiring more mutations which make the virus more infectious and result in more people dying.
I am referring to a drop in survival rate per infected person, because a virus changed in another way than becoming more infectious.

Welcome to the site. Please take a [tour] and visit the [help] to see what makes a good question. SE biology in particular values questions that make some attempt at indicating that the person asking has done some prior research attempting to answer the question themselves. So - what evidence do you have that some viruses become more lethal and that this occurs not because they are more infectious?

I think implicit to this question is that it is more beneficial for the virus if the host doesn't die. Could just boil down to statistics: More ways to go wrong than right so more likely to not coexist than coexist.

It depends on what is implied by over time in the question.
Virus may become more deadly (or otherwise harmful) simply due to a random mutation. However, virus does not specifically aims at harming the host - rather the negative consequences for the host's health are a byproduct of the virus hijacking and killing the host cells. This can be, e.g., due to the toxins generated during the viral replication, or due to the new virions bursting out of a cell and thus destroying it, or because of the overreaction of the host's immune system. E.g., HIV preys at the immune CD4+ cells, whose count eventually drops below the critical level, making the host susceptible to opportunistic diseases.
Thus, in a short run virus becomes more harmful/lethal, as the byproduct of being more successful in replicating and propagating itself. However, in the long run such success harms the virus, since, as an obligate parazite, it cannot exist without a host. Reduced number of hosts means reduced possibilities for virus to replicate. A virus that kills all of its hosts goes extinct. The viruses that continue exist do so either because they have reached an endemic equilibrium with their host or because they can survive in a host of different species, occasionally spilling into human population (like Ebola).

Sometimes, a virus may indeed benefit from specifically harming the host - a dead host may for example facilitate dispersal of virions.  A virus in the short run also may not become more harmful/lethal even if it becomes more successful in replicating. There are multiple levels of "trophism" involved depending on scale - subcellular, cellular, organ-level, whole organism, population, and kinetics may act against reaching an equilibrium state.  I think it's important to be specific about scale, time span, etc when asking such a question.

@Armand thanks, these are valuable points.


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Ways to distinguish between purifying selection and selective sweep
When looking a population genomic data, regions of low diversity (lower than expected; such as in a region of high recombination) can indicate either purifying selection of deleterious mutations or a selective sweep of an adaptive mutation. What are some ways one can tell which one occurred?
One way I've heard of is to use an outgroup that did not live through the same events as the main group. If the outgroup also has low diversity, it means nonsynonymous mutations in that region are deleterious regardless of events, and so those homogeneous regions likely underwent purifying selection. If the outgroup has high diversity in those regions, the main group likely went through a selective sweep.
What are other ways to distinguish between the two?

Welcome to Biology.SE!
I actually recently went through the literature on this and similar subject, so I'll be happy to answer.
The answer will not be easy to formulate as a number of authors are working and arguing on the question. I will try to give a quick overview of methods.
Definitions: Background selection and selective sweep
First off, let's use the correct terms. As you described, both positive and purifying selection is reducing genetic diversity at nearby loci. When the reduction in genetic diversity is caused by positive selection, we call the process selective sweep . When the reduction in genetic diversity is caused by purifying selection, we call the process background selection.
What affect background selection?

Recombination rate
Strength of selection.
For a given neutral locus at distance $r$ centimorgans from a locus under purifying selection, the selective coefficient $s$ that is causing the highest decrease in genetic diversity is $s=r$ (Nordborg 1997).
Mutation rate
population structure

What affect a selective sweep?

Strength of selection
population structure
Number of loci involved under adaptation
Whether adaptation comes from de novo mutation or standing genetic variation

By the way, you might want to have a look at the terms 'soft sweep' vs 'hard sweep' in relationship to the two last elements of the above list and in relation to local adaptation.
How to disentangle Background selection from selective sweep?
There are a number of technics but again all of that is a work-in-progress. I would like to classify these methods into four themes.

Environmental covariate

This first element talks about disentangling local selection from background selection. It is maybe not exactly what you asked for but this discussion often comes to center stage in the literature talking about both.
If we assume to know the environmental variable causing the adaptation, then you can compare divergence between population present in different environments and those present in the same environment. If loss of genetic diversity is caused by local selection, then divergence should be higher between population occurring in difference environments. If loss of genetic diversity is caused by background selection, then all populations will show similar divergence. Bayesian Technics such as BayEnv2 (Gunther and Coop 2013) take advantage of this technic.

Among lineages comparisons

By comparing related species, it is possible to find out regions of low genetic diversity. If all related lineage show similar loss of genetic diversity irrespective to the existence of an adaptive event, then the loss of genetic diversity is likely caused by background selection.
From such methods (but I might not totally understand them, I should read the paper again), some authors (such as McVicker 2009) have build B-map and recently implemented in BayeScan (Huber et al. 2016; BayeScan is an Fst outlier method to detect local adaptation), that is map of the genome of the intensity of background selection measured by the B-value introduced by Charlesworth (history of the term reviewed in Charlesworth 2012)

Allele-Frequency-Spectrum

Both background selection and a selective sweep affect the Allele-Frequency-Spectrum as to cause an excess of rare alleles (Tajima's D < 0). However, the strength of the effect and the detailed effect on the Allele-Frequency-Spectrum is not quite the same and some authors have suggested to use such differences to disentangle the two.

Machine learning (thank you @ atongsa)

Recently, there has been much interest in using machine learning techniques to develop methods to detect selection. For example, many people are performing numerical simulations of evolving populations and are training a machine learning algorithm to detect loci under selection. Hejase 2020 apply a SVM method and find a rapid avian radiation have been driven by recent selective sweeps. Hejase 2022 developed a Recurrent Neural Network (RNN) by using the Ancestral recombination graph to infer how selective sweeps shape genomic diversity.
Reading suggestions
There is a lot to read on the subject. I would recommend the recent special issue in Molecular Ecology DETECTING SELECTION IN NATURAL POPULATIONS including the review Haasl and Payseur 2016.

@user25375 Do you think I answered your question?

thank you, you give a great review of this question.  i am newbie, and i think 4. machine learning maybe good at distinguish such two selection process just by input huge data and build a good model for selection sweep and background selection.

@atongsa Good point! I suppose, that was not much of a thing back in 2016 when I wrote this answer but it has become quite a popular topic of research nowadays. I don't know much about it but I quickly added a fourth point above. Please feel free to edit if you can add more information and/or cite a few papers.


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How are electrodes working? (EEG)
How do electrodes receive signals from the brain when using/doing an EEG? Is there some "circuit" for it? Is it harmful if you have many (more than 50-100) on your head?
I found out that there are small disks used as electrodes to pick up the brain waves. What I didn't understand was how the circuit behind that worked. I mean each electrode has to have an individual circuit, right?

command to bump question

Welcome. What did you find out when you researched this question and what didn’t you understand? There is a lot of information about how EEGs work online.

Also please don't bump questions with meaningless edits.

I found out that there are small disks used as electrodes to pick up the brain waves. What I didn't understand was how the circuit behind that worked. I mean each electrode has to have an individual circuit, right?

The circuit is typically made with one or more "ground" wires for EEG, though it's possible to use other EEG contacts as references (more often this is done virtually - the original recordings are made and digitized with a common ground, and later an average reference or Laplacian is used to isolate more local signals).
EEG measures extremely weak signals and doesn't have any impact on brain activity itself, any more than listening to the radio impacts the broadcast tower.

Thanks for your answer. Is there any schematic for the circuit?

@Jakob An op-amp in your recording equipment with one wire to each EEG contacts and one to the ground wire.


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Should a red blood cell in hypertonic solution be drawn with a nucleus or not?
I'm a student at 6th stage in High school from Iraq. I need to draw a red blood cell when it is put in a hypertonic solution; "high concentration of solute and low concentration of solvent".
Do I draw it with a nucleus or not? I think there is no nucleus because the cell has a nucleus only when it is in the bone marrow, but it loses its nucleus later. So when it is put in a hypertonic solution that means it doesn't have nucleus. But my teacher said that it should have a nucleus.

Hello @handsomecat !! Welcome to Biology SE. Yes! you're right. A mature RBC doesn't have a nucleus. However, for this particular activity, the source of the blood sample has to been taken into consideration. If the sample was taken from a vein, the RBC should be enucleated. If the sample was taken from Bone marrow (generally Hip bone) then RBCs should be nucleated.

What species?  Human RBC don't have nuclei but some species' (for instance, birds) RBCs do.  May be the source of confusion.

The nucleus being absent is secondary to what happens with the cell when you put it in a hypertonic solution.  Perhaps you are studying osmosis?

Yes, it's the osmosis..thank you all.


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Can Shark bodies be preserved?
Under normal conditions, Shark bodies, which are made of cartilage are not preserved and only the teeth can only be preserved. I searched whether Shark bodies can be preserved in ice and I got this CNN article link about a megamouth shark. I'm guessing this was washed up or something, its preserved in ice at the Smithsonian.
I think sharks could encounter ice or some other preservative material and get trapped, like frozen saltwater, iceberg, or amber. So is there a definitive answer if shark bodies can get preserved in such material?
UPDATE
I realized frozen salt water would not be a preservative because sharks don't live near the polar seas and ocean, but that does not rule out the possibility of shark catching a current, because warm currents spread out to the poles, and cold water spread out to the equator.

https://www.google.com/search?q=can+amber+be+found+on+the+ocean+floor&rlz=1CASFJY_enUS951&oq=can+amber+&aqs=chrome.0.69i59j69i57j0l8.3723j0j7&sourceid=chrome&ie=UTF-8&safe=active&ssui=on

Do you mean preserved by some natural means, or by humans?  For the latter, you might read the rather amusing book "The $12 Million Stuffed Shark": https://us.macmillan.com/books/9780230620599

Natural Preservation.

Ahem, greenland shark locations...

Now I really want a shark preserved in amber… d***!

define preserved, there are plenty of whole body shark fossils.

Yes, it's possible if they are in very cold, low oxygen waters. Fossils of manta rays are fairly common, and there are examples of complete shark fossils preserved by silt and limestone.
Sharks can also be curated using epoxy, formaldehyde, alcohol and other preserving substances. There are famous preserved sharks, one is called Rosie, a great white from Australia, and the other is by Damian Hurst, a tiger shark.


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Hormonal effects of Luteinizing hormone on endometrium
What is the effect of luteinizing hormone on the endometrium?
A general answer to this query is that it only thickens it. The same could also be said for the effect of Follicle stimulating hormone (FSH) on the endometrium as well.
Where lies the difference?

Both FSH and LH are indirectly involved in endometrial thickening:

GnRH regulates release of the gonadotropins- luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from specialized cells (gonadotropes) in the anterior pituitary gland
LH and FSH promote ovulation and stimulate secretion of the sex hormones estradiol (and estrogen) and progesterone from the ovaries.
As estradiol levels increase, the intact basal layer regenerates the endometrium to its maximum thickness late in the ovarian follicular phase (proliferative phase of the endometrial cycle).     ...{1}

Again, wikipedia{2} says the same:

...In both cases, the endometrium initially proliferates under the influence of estrogen.

The difference between the hormones, of course lies in their other functions. You can see this for more on that. To clarify again, the endometrium does not thicken 'differently' under the influence of each.
{1}-https://www.msdmanuals.com/professional/gynecology-and-obstetrics/female-reproductive-endocrinology/female-reproductive-endocrinology?query=lh
{2}-https://en.wikipedia.org/wiki/Endometrium#Cycle

extending @Bipasha: (cant comment yet)

As the endometrium gets to the to the mid-cycle (ovulation), the LH surges, and the become more dominant in the "luteinising phase" of the ovary. In this phase, in response to the LH, the ovary secrete progesterone that "stables" the endometrium in the "secretory phase".
When the LH drops, the progesterone drops and the endometrium sheds. In clinical perspective it's called "progesterone withdrawal" and the principal used for fertility evaluation.
When the regular and timely mensuration occurs, its serves as an indirect indication that the endometrium "saw" estrogen (or other derivative as esterdiol) and later, progresteron.
In other words, in the right physiological fertile context, LH is indirectly stabilise the endometrium.


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Why do coronavirus cases graphs have a sinusoidal like shape?
Some screenshots from a canadian website:

See this sinusoidal shape? Why is it there? Shouldn't it be a single curve?
My main guess is when cases are counted: is it possible that they are counted something like every monday or so? I can't believe the virus progression really has sinusoidal-shaped curve.
It is not an error in the website, since other sources seem to show the same thing: worldometers, nbc news, and many others

I think you mean SINE, not SINUS.  They're different words, with different origins. https://en.wiktionary.org/wiki/sine#Etymology vs https://en.wiktionary.org/wiki/sinus#Etymology

@jamesqf The page you liked says that sine is a "Doublet of sinus". Hence, they have the same origin. And since the OP has a non-English name, they probably speak on of the many languages where the function is indeed still called "sinus". For example, https://en.wiktionary.org/wiki/sinus#Noun_7

I did mean sine, thanks for the info. The sine function is labeled "sinus" in french.

It's a weekly cycle due to reporting disruptions over the weekend.
Use a 7-day moving average to get a better picture. Holidays and such can still be disruptive but the 7-day average solves most of it.

That's what happened in the UK. Most hospitals didn't report on Saturday / Sunday / Bank holidays, a small number did. The results published were based on the reports of the day before. So Saturday result = normal, Sunday result = low, Monday results = low (because little got reported on Sunday), Tuesday results = very high (most of Saturday / Sunday got reported on Monday), Wednesday results = slightly high (some hospitals didn't manage to report everything on Monday).

And then we had newspapers that reported every weekend how we are beating the virus because the numbers dropped, and every Tuesday how we were struck by total disaster because the numbers went up.

authors: Vladimir F Героям слава


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How can we determine which chromosome came from which parent?
In this article there is a graph (figure 1) describing different levels of methylation in the maternal and paternal chromosomes after karyogamy.
How can the researchers identify which chromosome originates from each parent?

That article is a review, and cites two other reviews for this figure.  The more recent one is freely available and looks fairly thorough, with more direct references to primary publications.

A straightforward way to identify which chromosome came from which parent would be to use sequences of known fragments of parental chromosomes or to use SNP arrays. I hope that I did not miss your question completely.
Regards,

is that the common way? I learned this subject in a course where they also spoke of sequencing techinques including SNP arrays but they said that teaching how to recognize chromosome origin is out of scope so I assumed there is another way.


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How long does DNA last in wood?
I was wondering if it's possible to find out if the wood of the table I bought is from the same tree of the chair in the same set. Most likely not, but I was wondering if it's theoretically possible to get the DNA from both and compare them.
How long does DNA last in wood to the point that it's still useful for DNA comparisons? Are we talking about days, months, years, maybe longer?

I initially read the title as “a wood” and started wonder what crime was being covered up!

Even if you can get DNA, it might not be useful. I think in a lot of commercial situations trees are propagated by cuttings, which means two different trees could be genetic clones.

@TimSeguine Most timber from the northeast and northwest US comes from naturally regenerated forests. In the southeast, where most timber is produced on plantations, only a portion of plantations use cuttings.

DNA can remain intact in wood, enough to perform useful identification, for centuries (this study had success with wood from ~1300 AD). However, successfully extracting DNA from the wood may be difficult, depending on the species, age, cut, and preservation.


text:
What bug is this in my closet
I keep finding these little insects on my clothes in the one corner of my closet. They seem to be a mm in length. I’ve never seen them walk and I’ve only seen one in any given time. I’ve never seen hairy projections so it makes me want to rule out carpet beetles since the photos online show some hair. Tonight I found one on my fabric headboard. They seem light brown with black stripes.  Thoroughly disgusted. [

Hairy projections are only really found on the larvae of the carpet beetles.
The adult beetles look like beetles - which this almost certainly is.
Probably varied carpet beetle

Image attribution: Staff of York Museums Trust, CC BY-SA 4.0 https://creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons


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How to disambiguate between chromosome and chromosome pair?

Our genetic information is stored in 23 pairs of chromosomes that vary widely in size and shape. Chromosome 1 is the largest and is over three times bigger than chromosome 22.
Source: https://www.ncbi.nlm.nih.gov/books/NBK22266/

There are 23 pairs of chromosomes. But the article is using the phrase "chromosome 1" and "chromosome 22" to refer to "chromosome pairs".
What is the correct term here?
Is there a term referring to a chromosome class or type or something similar?

This is standard. For a typical human diploid cell there are two copies of chromosome 1, two copies of chromosome 2, etc; you'd have either two copies of the X chromosome or one X and one Y.
There's not really any ambiguity, the chromosome IDs are always a type or class in some sense.
See for example https://en.wikipedia.org/wiki/Karyotype

Is it because of the said ambiguity that in mitosis chromosome number remains constant till  anaphase and doubled after anaphase upto cytokinesis. Also  chromosome number is halved in meiosis 1 but DNA is  halved(again) in meiosis 2

I remember our teacher telling us that after DNA replication both sister chromatids are together called 1 chromosome but after sister chromatids separate each sister is treated as an individual chromosome


text:
Concept of mean systemic filling pressure
Mean circulatory filling pressure (MCFP) in humans was defined by Guyton as "the pressure that would be measured at all points in the entiere circulatory system if the heart were stopped suddenly and the blood were redistributed instantaneously in such a manner that all pressures were equal".
Now according to many physiologists, there must be a location in the vascular network where the pressure is completely independent of the cardiac activity, and this pressure must be equal to the MCFP. Apparently, this was already noted by Starling in 1897. The entire point is well explained in this article.
I have read this article and some others introducing the concept of MCFP to medical students; many of them report the same observations made by Guyton, Starling, etc., but a point which is never addressed is why there must be a location in the vasculature where the pressure is independent of cardiac activity.
I feel like getting a satisfactory answer to this question would greatly improve my understanding of hemodynamics, so I would be very grateful if you could explain the concept to me.

You've misread the linked article if you take this to mean there is some place that is unaffected by cardiac activity. It's just that there must be some place that is equal in pressure to the MCFP. The actual position fluctuates throughout the cardiac cycle.
The reason, though, that some place must be equal to MCFP is that pressure is continuous. Somewhere in the vasculature (i.e. proximal arteries) is definitely greater than the mean; somewhere else (i.e. proximal veins) is definitely less than the mean. Because the pressure varies continuously the function must pass through the mean at some point along the vascular path. This isn't anything special about biology, just mathematics.

Thank you very much for your answer. I am well aware that, if MCFP is comprised between mean arterial pressure and right atrial pressure, then there must be a point in the vasculature at which pressure equals MCFP. But the article I mentioned seems to say that this point does not move with cardiac activity, as illustrated with the fact that the three curves in figure 3 intersect at a unique point. This is stated even more clearly in Rothe (1993), a work cited in the article.

In Rothe (1993) the authors, citing Starling, state "Somewhere in the circulation there must be a point where the pressure is neither raised nor lowered and where, therefore, the pressure is independent of cardiact activity."

@user47679 "Rothe (1993) thought that this probably happens in small venules (less than 1mm diameter), and that it is not constant - present at different points of different organs, and changing constantly depending on prevailing conditions" - quoted from your source.

They're talking about a hypothetical location that's constantly shifting. I think you're reading too much into it or taking it too literally.


text:
Is there any data on Neanderthal admixture in Western European Hunter Gatherers?
If there is any data, was the rate of admixture higher than today? Like WEHG brought the component in? Or was the amount maybe lower, like other groups like Early European Farmers or Yamnaya brought the admixture? Or was it evenly distributed?

tldr; Neanderthal ancestry is roughly equally the same between the groups you mentioned.
It's almost certain that the major pulse of Neanderthal admixture into non-Africans occurred very soon after the primary out of Africa event (here I am referring to the out of Africa migration which contributed towards most of the ancestry of all non-Africans today - of course there were other out of Africa migrations which were effective dead ends).
This is well established from a) looking at the size distribution of Neanderthal fragments in the human genome (ref, ref) and b) the fact admixture occurred around 232–430 generations before the 45kya year old UstIshim individual was alive. So most lines of evidence suggest this admixture took place between 50-60kya.
This is much earlier than the diversification of West Eurasian populations into groups like Yamnaya, Anatolian farmers and Western Hunter Gatherers. Therefore, there is no reason to expect any one of these ancestral groups would have had higher amounts of Neanderthal ancestry than any others, since the admixture event occurred into the common ancestor of all these populations.
Indeed, from Haak 2014:

The ancient individuals had indistinguishable levels of Neanderthal
ancestry when compared to each other (∼2%) and to present-day
Eurasians (Supplementary Information section 6)

There are some ancient individuals such as Oase1 who carried substantially more Neanderthal ancestry than modern day samples (in fact this individual has very recent Neanderthal relative), but that they didn't contribute anything towards the ancestry of later groups.
Btw I know a lot of these reference are old - I will add some more recent estimates later, but they don't change the overall picture.


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Unknown plant, please help me identify it
Years ago I was into keeping tropical fruit trees/bushes indoors. One of them didn't do well under my care so I planted it outside to enjoy the final year before European winter gets it. It somehow survived, barely. Each year it did better though so 5-6 years later it's full of edible fruit. I don't know what it is. Can somebody identify it?

is it this: https://www.youtube.com/watch?v=KTYMG7mziRw ?

The fruit looks a lot like something from the Syzygium genus. Can you show us a cross section (lengthwise) of the fruit?

@JimN I think you may be correct.

crush one fruit, see if it has flesh crunchy like apple - if so probably Syzygium

It worries me a bit that you don’t know the species, yet you know the fruits are edible. I hope you simply remember it’s supposed to be edible when you first got the plant?

JimN, yes that was it. Jujube (Chinese Date). Some variant of it

It appears to be a cultivar of Jujube (Ziziphus zizyphus) also known as Chinese date - https://en.wikipedia.org/wiki/Jujube
This is based on JimN's correct observation. I looked at a few dozen images of Ziziphus Zizyphus - both fruit and leaves. They appear to be identical. The fruit tastes as described. The fruiting progression matches the description in Wikipedia.

You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— You may also wish to consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

I understand where you are coming from but what you are suggesting is an online form of politics and bureaucracy (time-wasting). I will edit my answer to oblige


text:
Is an axillary bud a type of intercalary meristem?
I have read that some cells that are left behind from the shoot apical meristem constitute axillary buds and that these are capable of forming a branch or a flower.
So will the axillary bud also be called a meristem? And if so, will they be called the intercalary meristem?


text:
Help identifying organism
I would like help identifying this "crab".
I looked through 32 pages of crabs on this resource http://species-identification.org/ but none of them look like this little animal found in the waters of Madeira.
They move fast and are something in between a spider and a crab.

It is definitely a crab - not anything spider. I originally thought it was a Sally Lightfoot Crab (a common crab on Madeira from the family of shore crabs) but I agree on your comment that it is more likely a Nimble Spray Crab (of the Flat Crab genus) as the specimen in your photo seemed a lot flatter than a shore crab (but I wasn't sure if it was just the shape of the rock).
The Wikipedia article on this species says that these are also referred to as another kind of Sally Lightfoot crab, and the fact that these are in a different taxonomic family from the other ones (the shore crabs) is a topic of debate.

They are observed in the coastal Atlantic and considered native to Madeira, but have recently spread into the Mediterranean

You can view a gallery of almost 200 photos of these crabs on iNaturalist.

According to my dive instructor and to these pictures: https://inaturalist.ca/taxa/61372-Percnon-gibbesi/browse_photos it indeed is a kind of Sally Lightfoot, specifically it's the Percnon Gibbesi (Spray Crab). Thanks. If you edit your answer to reflect this I'll accept your answer.

Thanks for the clarification - edited to reflect your feedack


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Cell culture media L-Glut dilution?
Cross-posted on r/labrats.
I haven't done cell or tissue culture in about 4 years.
Protocol:
Volume: 200ml media (academia so using sparingly, not the whole 500ml bottle!)
1% L-Glut (250uM)
My L-Glut comes in a 100ml bottle of 200mM.
What should I make up a stock dilution of 250uM in? Distilled H2O? PBS?
Should I then add 2ml (1%) to my media? Or should I add 250uM of L-Glut directly to the media?


text:
Why does the sandalwood tree produce a fragrant oil?
Why do sandal trees produce fragrant oil? Is there any purpose for it? Is it to make it unpalatable for other herbivorous animals? If so, why do humans find the fragrance pleasing?

Probably the same reasons as lavender, sage, vanilla, lemontree, jasmin, thyme, and other plants used for extracts. They generally protects the plant and aromatic effect is a coincidental side effect for our species. Catnip is an odd example of aromatic side fx.


text:
How does one derive a KD from an equilibrium titration experiment?
If I have an antibody A and a target B, and experimentally titrate the antibody against a single concentration of B, and then measure the % of B that is bound after the solutions reach equilibrium, I should be able to determine the KD of the interaction.
Source below (and others) shows that determining KD is as simple as determining the EC50 of such a curve. Source.

How does that square with the following equation for KD?
$KD = \frac{([A]*[B])}{[AB]}$
where A is unbound antibody, $B$ is unbound antigen, and $AB$ is the bound complex.
Let's say I have 10 pM of target antigen, 50% of which is bound when incubated to equilibrium with 10 pM of antibody. That would mean the antibody and antigen are each 50% bound and 50% unbound.
$KD = 5pM * 5pM / 5pM$
$KD = 5 pM$
So I have calculated a 5 pM KD, not the 10 pM that I would think would be similar to the graph below (assuming they had pM units on the X axis) I'm assuming these types of example graphs refer to the input concentration, right?
Even more confusing, what if the antibody is a really tight binder, such that 10pM of antibody is able to essentially bind 100%, such that 10 pM antibody is able to bind 50% of 20pM of antigen. (1:1 binding assumed)
$KD = ~0.001pM * ~10pM / ~10pM$
Now you have a KD of 0.001pM, but the graph would suggest that 10 pM of antibody is necessary to bind to 50% of the target antigen.

Welcome to Biology.SE. Unfortunately, general chemistry questions without a strong biological component are off-topic. Just mentioning enzymes or antibodies as reactants isn't sufficient. Please delete your question here and ask it at [chemistry.se] (cross-posting is frowned upon), or flag it and request that it be migrated.

Are you sure? Protein-binding, which is definitely the most relevant tag, is not even an option in the chemistry stackexchange.

The models you are using are based on the Langmuir Isotherm. The classical use of this model is for gas adsorption to a solid. In these experiments, the pressure of the gas is measured against the fraction of sites bound.
This model is easily transferred over to aqueous systems, but you have to be careful about making the correct analogies. The pressure of the gas is related to free concentration of the gas, not the total concentration. So the X-axis of your plot must be the free concentration of your ligand.
Most experiments are done where the ligand is in major excess of the receptor. Therefore, the free ligand concentration is roughly equivalent to the total ligand concentration. However, when this isn't the case it is not hard to adjust based on a known ratio of ligand to receptor.
At 50% binding we know that:
$K_d = [L_f]$, where $[L_f]$ is the free concentration of ligand
From conservation of mass we know:
$[L_f] = [L_t] - [LR]$, where $[L_t]$ is the total ligand in the solution and $[LR]$ is the concentration of bound ligand
Since we are at 50% bidning we know:
$[LR] = \frac{1}{2}[R_t]$, where $[Rt]$ is the total receptor concentration.
This lets us solve:
$K_d = [L_t] - \frac{1}{2}[R_t]$


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Apparant inconsistency in DNA topology theory in formation of origin of replication
I'm studying an introductory course in genetics and came across something I don't fully understand. I obviously used Google to find where I'm thinking wrong, but I still can't understand it.
To catalyse strand separation, a negative supercoil is introduced due to the binding of DnaA-proteins, so the strands aren't being broken to form the supercoil. This means that the linking number must stay the same. Due to the negative supercoil the Writhe is decreased by 1, and thus the Twist must increase by 1 (because Lk stays the same).
A higher twist means that the DNA strand is overwound. Meanwhile my Textbook says this negative supercoiling implies underwounding.
Where am I wrong in my thinking?

Does this answer your question? https://biology.stackexchange.com/questions/54059/why-is-compensatory-negative-supercoiling-generated-in-a-positively-supercoiling/