text:
Why does increasing the space constant increase conduction velocity in myelinated neurons if nodes of Ranvier are constantly spaced?
If depolarisation at one node of Ranvier triggers, by passive conduction, an action potential at the next node of Ranvier, why does increasing the space constant increase conduction velocity? Surely the locations of each action potential are pre-determined by the sites of the nodes of Ranvier? Is it simply the rate of the passive conduction that changes?

I think the simplest answer to your question is that you're correct in thinking passive flow would be what changes, but the reason behind it is important to understand.
I'd recommend looking at UT Health's neuroscience online resource where they break down action potential propagation in an understandable way. The main takeaway is that the space constant is determined by a number of different physical characteristics of the neuron/axon. You can find these characteristics at the link I provided, but the three parameters that define the length constant are diameter of the axon (d), membrane resistance (Rm), and axial resistance (Ra).
Starting with Rm (because you allude to myelin in the question), this is dramatically affected by myelination. An internode (the myelinated portion of an axon in between nodes of Ranvier) has an excessively high Rm, which just means that current doesn't readily flow across the membrane, so current doesn't "leak out" while it's passively flowing down the axon here. Therefore, increasing Rm by lengthening internodes would help increase the distance across which current can passively flow in the axon (which increases the space constant). Shortening internodes would have the opposite effect. However, you seem to be asking "All things with myelin remaining the same, why would a higher space constant increase conduction velocity?"  That's where d and Ra come in. I explain these below:
The values of d and Ra are somewhat linked. Basically, a high the value of d allows passive current to flow more easily along the axon, meaning it has a low value of Ra. So in the context of your question, if you had an axon and theoretically doubled the axon diameter (so from d to 2d), Ra is cut in half (so from Ra to Ra/2) and passive conduction can speed up. This would increase the space constant by its effect on passive conduction. The converse is true if you shrink the axon diameter. However, it's important to realize that Ra can also be affected by other factors like the contents of the cytoplasm in the axon. That is why both are used to calculate the space constant even though they relate to one another.


text:
Why can DNA tests with mixed DNA of several people not be used to detect a criminal in a database?
Scenario: Two males attack another pair of two males with a weapon. The attackers are fought off and the weapon remains. Why does the police require DNA samples of the two who have been attacked to be able to find out if the two attackers are in the national criminal database?
Or without the specific scenario: Can a DNA profile be created from a sample where several individuals have been involved and it is not possible to separate the cells and assign them clearly so that this profile can then be searched for in a database?
Disclaimer: This happened to me and several years later, I'm simply curious why I had to give a sample to help police find the perpetrators.

source: Stack Exchange

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

sort: votes


text:
How to color based on b-factor for all the frames in one object in Pymol?
I load a protein.pdb file into Pymol. This file has multiple frames (or states), and with different b-factor values at different frames at the PDB file b-factor columns.

After running the spectrum b command, the colouring is only based on the last state of the object.
So can I colour the frames differently using their corresponding b-factor values? In that case, I can see the colour changing throughout the frame playing.
In case someone wants to create a PDB of multiple frames, you can do like this:
MODEL        1
ATOM ......
ATOM ......
ENDMDL
MODEL        2
ATOM ......
ATOM ......
ENDMDL

Do you have a PDB ID one could use to reproduce this?

The PDB downloaded from the PDB website usually has only one frame. But my PDB comes from molecular dynamics, which has multiple frames. You can simply add a line of "MODEL        1" before the content, then add another line of "ENDMDL" at the end, and repeat this multiple times to create a PDB with multiple frames

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


text:
Expected number of SNPs in a sample of size `k`
Consider a Wright-Fisher population of constant size $N$. We sample $k$ haplotypes in this population. What is the expected number of SNPs?
I think the answer should be in Watterson (1975) but it looks like my institution does not pay for access to this journal.

Try using Sci-Hub.

Let $\theta = 4n\mu$, then $E(S) = \theta\sum\limits_{i=1}^{k-1}\frac{1}{i}$, assuming infinite sites model. This is indeed given by Watterson (1975).


text:
How much oxygen does a brain consume?
I am not a biologist - my background is in quantitative sciences, and I am trying to answer a rather quantitative question:
How much oxygen does a brain consume?
This however raises many sub-questions of purely biological nature:

How is the brain supplied by oxygen? (My naive understanding is that lungs tie oxygen to hamoglobin, which is then carried by blood to cells, which then ingest the oxygen, converting it to ATF. Is this correct? Does this apply to neurons as well?)
How much energy a neuron or the whole brain consumes per unit time? (e.g., per hour, in energy units or oxygen content)

I will appreciate explanations in laymen terms or references to accessible literature.

https://www.dentinstitute.com/posts/lifestyle-tips/22-facts-about-the-brain-world-brain-day/ #16.please do a tiny bit of research before asking it here.

@trondhansen I've been doing research, and the link that you sent is a bit lightweight -  e.g., it says nothing about blood-brain barrier. Also, I need to see the numbers - e.g., how much energy does brain consume in Joules or kcals per hour?

As has been commented, the answers to some of the questions here can be found in the literature. The nutrients and oxygen reach all tissues by the circulatory system — i.e. in the blood. And the link supplied by @trondhansen suggests a litre of oxygen a day. (I wouldn’t know — I never studied physiology.) However, as regards energy, I supply the following from the biochemistry text, Berg et al.

Brain. Glucose is virtually the sole fuel for the human brain, except during prolonged starvation. The brain lacks fuel stores and hence requires a continuous supply of glucose. It consumes about 120 g daily, which corresponds to an energy input of about 420 kcal (1760 kJ), accounting for some 60% of the utilization of glucose by the whole body in the resting state.

Note the correct form of expression:

the brain  / consumes fuel / to generate energy / to perform ‘work’

Glucose is the fuel, ATP is the chemical energy currency, and the work performed (as the text makes clear) is for the main (60%–70%) to:

maintain the sodium/potassium ion membrane potential required for the transmission of the nerve impulses.

(I am afraid that’s about as layman’s terms as I do. It does say on the label that this site is for students of biology.)

Thank you for the explanations and for the reference (I have found a similar number - that brain consumes 20% of the total daily energy intake, which is about 2000 kcal.) Do I understand correctly that neurons receive both the sugars and the oxygen via the blood stream as raw materials, and convert them to ATP, just like any other type of cells?

Yes indeed. However cells are different in the way that the hormones of the fed and starved state affect the uptake of glucose through the cell membrane. This is done by transporter proteins. For tissues that can use other fuels in starvation, insulin is required by the transporters to prevent them using glucose, which is prioritized for the brain. The brain transporters are subtly different, in that they do not require glucose. The ATP generation is the same.

The project that I am working on actually presupposes using liposomes as a method for delivery of extra (Hb-bound) oxygen to the brain. From what I read, the liposomes are necessary for overcoming BBB (blood-brain barrier) which is inpenetrable for most drug-delivery methods. But it seems that this also raises the question of supplying additional sugars...

I don’t really know. I would doubt you could or would need to do that. Glucose uptake is usually a pull method in response to demand.


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Pectoralis muscles as push muscles vs pull muscles
Pectoralis muscles are the adductors, flexors of arm in addition to medial rotators  of arm. How does this action translate in to acting as helping in push ups or in bench press?
I am having trouble visualizing the primary actions helping in these compound movements.
I also have trouble understanding why this muscle being a powerful adductor does not work in pull up exercise?

The pectoralis major is not just an adductor and medial rotator of the arm. Its clavicular fibres also flex the arm at the glenohumeral joint. This is the action useful in performing push-ups and bench presses.
And yes, its adductor action also plays a role in pull-ups and climbing (along with that of the latissimus dorsi, another adductor).

References and further reading:

https://www.kenhub.com/en/library/anatomy/major-pectoralis-muscle

https://www.kenhub.com/en/library/anatomy/the-shoulder-joint

Romanes GJ. Cunningham's manual of practical anatomy. 15th ed. Vol 1, Upper and lower limbs. Oxford: Oxford University Press; 1986. (ELBS edition, 1989 reprint). 263 p.


text:
Can viruses be deformed?
Viruses are created in their fully-formed state and do not grow. But one thing has been bugging me lately:
can a virus be deformed, e.g. in order to fit into an opening slightly smaller than itself? Say you were to apply a force to the virus perpendicular to the smaller hole; would the virus merely break, or is it possible for it to deform and retain its structure on the other side?

It would depend upon the virus.

Most viruses of human concern are "enveloped", that is, they are surrounded by a lipid membrane. This membrane is usually what determines the shape of the outer layer, and is intrinsically flexible, so most human viruses would be able to deform a bit to fit through a hole. Additionally, the size of individual enveloped virus particles tends to vary quite a bit as seen in this image from a previous answer:
You can also see that biologically active proteins stick out of the membrane. These are likely to break off if the virion experiences any significant forces. My experience with coronaviruses has been that even relatively mild purification procedures remove the spikes from most particles, let alone forcing them to deform through a hole. So, while they might pass through a small hole without rupturing, it's likely their ability to infect cells would be greatly reduced.
In the case of non-enveloped viruses such as adenoviruses or picornaviruses, their outer layer is composed of many copies of a "capsid protein", linked together according to quasi-equivalence. The capsid proteins need to join together over a range of angles, so they should be able to tolerate some flexing. Again, though, any extra proteins that stick out for biological functions (such as the adenovirus' fibers) will likely be damaged or detached, which would remove the virus' ability to infect cells.


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Ferns: How big can a circular sorus be?
I looked at some small ferns under the microscope. The circular sori of the ferns I looked at were less than 2 mm in diameter. The microscope I used had rather weak magnification, so I didn't get to see lots of detail. Later, I came across an image of large sori Wikipedia:

Image source. License: public domain.
I am surprised by the size of the circular sori in the image. If I could obtain large sori such as these, I would probably be able to see more detail under weak magnification. I'm wondering:

How big in terms of diameter can circular sori be?

What are some species of ferns with large sori?

Try members of the Asplenium genus, particularly the widespread Asplenium trichomanes or Maidenhair fern.
Without a location in the world, it will be difficult to give you a more specific answer.
Sori can be a few millimetres across, I would hazard a guess at about 5 mm diameter in my experience, but I have no scientific backing for that as a maximum dimension, and I'm only really familiar with plants in my country so can't make assumptions about other locations.


text:
Is a virus a poison?
I've understood that a virus is not a living organism (like e.g. a bacterium). From Wikipedia I get that a poison is a substance that reacts physically or chemically with molecules in the human body. Since a virus is a protein that binds to certain cells in the body and alters the cell's function in a harmful way (resulting in the production of more viral matter), why is a virus not a type of poison? (Or is it?)
Additional info:
I'd like to understand the difference between them—if any—on a chemical and physical level, as well as the consequences for treatment. For example: we all know by now that viruses can only remain harmful/intact on surfaces for a certain amount of time. However, I would think that a poison on a surface does not have such a time limit (but I may very well be wrong). What's the difference, if there is one? Why is licking a banister with viral load older than 4 (or so) days not harmful, but is licking a banister with poison older than 4 days?

Does poison have genetic material or can it divide like virus? Is it considered living when inside a cell, like viruses?

I am voting to close this question as it is about the use of the English language, not about biology.

@David I'm very confused by your attempts to shut down questions about viruses. Before posting I had also checked this relevant question and you did the same there. I initially wanted to post this to MED or Chemistry but according to WP, both poisons and viruses are in the realm of biology. Your suggestion of sending this off to a linguist is strange and absurd.

I see this as a valid question about terminology in the field of toxicology, which can be rather specific and sometimes inconsistent withing the field, and with common usage of similar terms in the English language.

Welcome to Biology.SE! Your question is about definitions — i.e. word usage. That seems sufficient to explain the comment by @David. As a new user please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. From that you will see that questions should be focused, that separate questions should be asked separately (not mixed together), and that we expect evidence of prior research, especially for something that meets the criteria for "homework". Thanks!

@MikeyC — The poster's doesn't mention that she is a student of toxicology, but I suppose that it is the question rather than the poster's intent (she doesn't make that clear) that is important. But if you regard this as question in toxicology, do you think it is of any importance to biology or the concerns of SE Biology? Is it related to some "actual problem she/you have faced"? And does some definition used by professional toxicologists (one no doubt you could link to) have any relevance to the average biologist, let alone person? Really?

Thank you all for the info. I still don’t really understand how we got to semantics but that may be my inexperience with both fields. I asked the question assuming scientific words have fixed objective meanings so different words denote different physical systems/objects/interactions. (Rather than denoting connotations etc.) I’m very surprised that does not seem to be the case for poison/virus but I guess this is part of an answer to the question then :) I don’t understand though why two fields of study exist (virology and toxicology) if the difference between them is purely semantic.

@David — Are you asking if the language used by biologists is of any importance to biology? "Really?" The fact that you suggest a formal definition used by specialists has no relevance to the average biologist/lay person underscores the importance of this kind question. Scientific jargon can obfuscate the intended message from non-specialists, especially when it overlaps with but differs in meaning from common parlance.

@Laura — I can see how it might seem like a purely semantic distinction, but it becomes meaningful in an interdisciplinary field like toxicology, which often overlaps with other biological fields like immunology and infectious disease. If we didn't have a convenient way to distinguish infectious biological agents (like viruses) from the poisons they sometimes produce, it would quickly get confusing trying to describe the mechanisms of disease etiology in a clear and concise way.

@MikeyC — No. I am asking about the one specific case of a word that long predated modern biological science and does not describe any biological process, and I doubt whether you will even find in a textbook of biology, except perhaps tangentially. This is a common word in the language of which everyone has an interpretation from centuries of usage. I am asking how knowing the particular definition a specialised field like toxicology has adopted will help with a real biological problem she has encountered, (A student preparing for an exam does not hack it. And her bio says she’s a physicist.)

Although "Virus" literally means "Poison" in Latin, it would be a great over-simplification to regard a Virus as a Poison.
Now, most poisons are chemical compounds that interfere in some chemical pathway in our body. For example:

Carbon Monoxide: Binds with Haemoglobin, rendering it unable to transport oxygen
Sarin: Indirectly inhibits degradation of the  neurotransmitter "Acetylcholine"
at the synaptic cleft.   Mechanism of action of Sarin

Hence most poisons are quite "simple" in their actions. However, viruses can be considered as a complex machinery of functions that interfere with a multitude of processes in our body including cell transcription, receptor-mediated endocytosis, et.c
Hence, the best analogy would be to consider a virus as a tactical poison.
Now, as for last question, viruses are fragile assembled structures.  Viral Self-Assembly

Environmental factors like heat, uv-light, oxygen, etc may damage the assembled structure. Hence, viruses have a self life, and so do may poisons.
  Sarin (self life)
However, poisons tend to have a longer self life because chemical compounds are more stable than the capsid of viral proteins with weak hydrogen bonds.
As per David 's suggestion, poison is defined as "...substances that cause death, injury or harm to organs, usually by chemical reactions or other activity on the molecular scales, when an organism is exposed to a sufficient quantity."  Wikipedia
Viruses do work at molecular level, but not in the same sense as poisons do. Hence, viruses do fit into the description of poisons but not precisely.
Hope you find this helpful.

What is your definition of "poison" and the basis for believing it is correct or universally applicable?

Thanks a lot for this and the examples. Sorry if this is a misguided question but are there any non-viral or ‘simple’ poisons that are transmissible in the same way a virus is? It seems to me a virus is unique in that one of its tactics is causing replication of itself, making transmission possible because of the sheer quantity of the substance in the body. Is there a toxin that can do the same?

The closest example that I can think of are Prions, which are just misfolded proteins molecules. Synthetic prions can be aerosolized and used as a slow poison . They cause a cascade of  protein deformation, leading to a slow neurodegenerative breakdown. They are naturally transmitted via cannibalism of eating infected mammalian brain in general.(https://www.defenceiq.com/air-land-and-sea-defence-services/articles/prions-as-bioweapons)

Virus is more complicated than just a protein. Rather it is a collection of proteins and nucleic acids (the viral genome), packaged in a certain way. When virus penetrates a cell, it hijacks the cellular machinery, making the cell produce many copies of the initial virus.
Unlike a cell, virus does not have all the necessary elements for reproduction, i.e. for copying its genome, generating all the necessary proteins, and ingesting food for powering this reproduction activity. This is why one says that viruses are not alive, whereas cells are alive. A cell can exist and reproduce without virus, but not vice versa.
A poison can a simply a small molecule (not necessarily an organic one) which is capable of disrupting normal functioning of a cell, e.g., by binding to some of its proteins.

What is your definition of "poison" and the basis for believing it is correct or universally applicable?

@David I wouldn't dare yo give any definition that is universally applicable

Is a virus a poison?
In toxicology, a virus is not classified as a toxic agent or a poison but as a biological agent (regardless of whether you consider it to be living or not). With the main distinction being the biological agents reproduce. You can find different definitions of "poison" in different sub disciplines of toxicology, but generally it's any substance capable of causing toxic effects in relatively small quantities. A "substance" in this case is considered to be a single agent. Just as salt-water is not a single substance but a mixture of substances, a virus is a structured organism made of proteins, nucleic acids, and other macro-molecules. Its often the case that none of these different parts are solely responsible for the toxic effects of a virus, but instead it's the action of viral replication which causes cellular damage leading to disease.
There are some biological agents which also produce toxins or poisons. One example is Clostridium tetani. This organism can infect an open wound, but it's toxicological effects are not a result of direct tissue damage caused by the organism, but of the tetanospasmin toxin it produces, which is a potent neurotoxin and the causative agent of tetanus. Again, in this case, C. tetani is the biological agent, but tetanospasmin is the toxin/poison.
we all know by now that viruses can only remain harmful/intact on surfaces for a certain amount of time. However, I would think that a poison on a surface does not have such a time limit
Neither statement is universally true. There are viruses that can remain infectious for months in the environment, and some bacterial spores that can survive for years. There are also some insecticides (poisons for insects) that breakdown in a matter of days in the environment. It just depends on the specific properties of each different agent, and on the environment they are in.

You mention the scientific discipline of toxicology, but — like the other answers — argue an opinion rather than cite a definition of "poison" and explain its practical relevance.

I provided a definition of poison, and discussed it's relevance to the question.


text:
What is this long cylindrical white fruit called?

Location: West Bengal, India
Temperature: 27 °C
Weather: Survive all seasons, although it was raining today
Length: 35 cm (although it can be small or big typically 10 to 40 cm length), girth:10 cm
Weight: 1 kg (estimate)
Appearance: Cylindrical in shape, the outer shell is very hard, color  of shell is typically white to pale yellow(the dark patches is due to mud and dirt). It is really tough to crack the shell but the inside (I believe) is pulpy and fibrous but dry.
Extra information: Not edible (never tried to eat), no smell emitted, colloquially called "monkey's club"(in native language), typically hangs on branches of trees in groups (typically 4 to 6 together)

is it the same as these white things in the foreground of the picture? https://www.thestatesman.com/wp-content/uploads/2020/01/QT-vegetable-production.jpg

Could it be Kigelia? https://en.wikipedia.org/wiki/Kigelia#/media/File:Kigelia-Africana-Fruit.JPG Native to africa, but seems to grow in a lot of places including mexico and india: https://inaturalist.ca/taxa/81491-Kigelia-africana/browse_photos?term_id=12&term_value_id=14

@JimN you are almost certainly correct, make it an answer!

It appears this is a Kigela (and commonly referred to as a "Sausage tree" in English).

It is - as you suspected - considered inedible and even poisonous in its fresh form (but apparently it can be dried or fermented). It has, as you said, a hard shell which can make this fruit usable as a container after it is hollowed-out.
The wikipedia article on this tree says it grows throughout tropical Africa, but looking at iNaturalist, it has been observed growing all over the world:

It's nice to have another naturalist here. There are a few of us, but I haven't been around much lately to have seen your answers. Very nice!


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Sequence of DNA
While giving an amateur reading to DNA. I was stuck within the first few lines:
Refined resolution of the structure of DNA, based on X-ray crystallography of short synthetic pieces of DNA, has shown that there is a considerable variance of the helical structure of DNA, based on the sequence. For example, a 200-bp piece of DNA can run as if it were more than 1000 bp on an acrylamide gel if it has the right sequence. The double helix is not the same uniform structure.
What does this highlighted portion mean?

Please provide a source for your quotation. The English is slightly strange, especially the last sentence. I think I know what it means, but an answer would be more useful if the context were provided. Your title should probably be something like "The effect of base composition on the structure of DNA", if this is indeed what it is about.

DNA sequence is what we call a string of nucleotides in the DNA polymer, such as GATTACA, representing a chemical structure wherein each letter ("G", "A", "T", "T", "A", "C", "A") represents a nucleotide that has a chemical bond to the next nucleotide. Possible nucleotides in DNA are adenine, guanine, thymine, and cytosine, e.g. A, G, T, C (you may also see such terms as thymidine, thymosine etc. depending on what piece of the DNA molecule you're talking about). What such a sequence implies for double-stranded DNA is that those nucleotides are then hydrogen-bonded to another "reverse complement" sequence, which for every nucleotide in the first sequence has a "C" for every G, a "A" for every T, a "G" for every C, and a "T" for every A. One way of representing this would be as follows:
GATTACA
|||||||
CTAATGT

Where | represents a hydrogen bond between the two strands of DNA at each nucleotide. A single-stranded DNA however would not have the H-bonds or the (lower) complement sequence.
Altogether, this is what is implied by DNA "sequence", though normally we only write GATTACA for simplicity.
What your quote means is that GATTACA can have a different behavior in a polyacrylamide gel than GGGGGGG or ATATATA or CCGGCCG, or any number of other 7-nucleotide DNA polymers. This has to do with the shape of the different nucleotides, each of which has a distinct chemical structure:

Some of the nucleotides force the DNA polymer molecule to take on different shapes, or to be stiffer or more flexible, because of their underlying chemical shape.
A polyacrylamide gel is basically a big tangle of polyacrylamide molecules and bonds. So think of DNA moving through it like trying to drag a rope through a forest. A very long rope will tangle more than a short one and will take more effort/time to pull through the trees. However, a rope of the same length that has a different structure (maybe it has lots of knots tied in it, or it is stiff rather than flexible) may also be harder to pull through the forest, even though it's not any longer.

I like your analogy in the last paragraph. I might borrow it...

@MattDMo thanks! it is my go-to for any kind of electrophoresis. There's a professor at UNM, maybe emeritus now (I forget her name... just saw a talk one time) whose whole thing is to think of all the tiny molecular stuff as happening on a spatial scale that is similar to our environments ("walk into a cell. what do you see?"). I think she's very right that that makes a lot of this stuff click in human brains.

It means what it says.
DNA runs through a gel at a speed which is due to its shape, which is mostly determined by its size.  What it's saying is that certain sequences alter the shape of the DNA so much that its passage through a gel resembles that of a much longer piece with a more standard helical shape.

Does it mean this: that a 200bp DNA can run at slower speed as if it is a 1000bp DNA, if it's sequence is altered in a certain way.    WHAT DOES THE RIGHT SEQUENCE MEAN IN THE SECOND LAST SENTENCE.?

@Arjun Tilak It means that some sequences can make the DNA take on different shapes like sequences with lots of G can form G quadruplex structures. https://en.m.wikipedia.org/wiki/G-quadruplex#:~:text=In%20molecular%20biology%2C%20G-quadruplex,one%2C%20two%20or%20four%20strands.

@ArjunTilak Avoid using strings of all-caps like that. It is perceived as "shouting" on the internet and can come across as quite rude.

@BryanKrause ok sir!! I am new at this site,will keep in mind!


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Recombination Data Set
I was looking over some genetics question and came across this data set.

In the fruit fly Drosophila melanogaster there is a dominant gene b+ for grey body color and another dominant gene c+ for normal wings. The recessive alleles (b,c) of these two genes result in black body color and curved wings respectively.

The question asked about calculation of the recombination frequency.
To me Ada's data set makes sense as the parental type offspring numbers are higher than the recombinant offspring. However, Donald's data set doesn't. Is there any way a recombinant offspring could be in a higher proportion than the parental type offspring?

can you give more info? which is the parental type? what is the experimental design? are these derived from the same background? what generation, e.g. F2? not enough info to answer as it is. This looks to me like a homework question, if so please add the "homework" tag.

This isn't a homework question. In fact, this is a question from IBO. I'll actually post the whole information.

b+/c+
b/c
b+/c
b/c+

Ada
~0.39
~0.42
~0.08
~0.1

Donald
~0.09
~0.09
~0.4
~0.41

The other chromosome beeing b/c (I assume each one got an heterozygote fly and than they did a testcross)
There are a two possibilities for an heterozygote fly:
(b+/c+, b/c), (b+/c, b/c+)
If there was no genetic linkage we would except 0.25 for each fly group, but we didn't which means that fly groups with a higher probability are showing the original parental chromosomes phenotyping.
Since they didn't get the same results (by far) I assume (there are statistical tests for this) each scientist got a differently genetic fly
Donald got (b+/c+, b/c) since in his experiment the predominant flies are those showing a dominant phenotype and recessive phenotype and Ada got the mixed fly.
With this in mind we can see that the recombination frequency is 0.18 or 18cM
Yes, the recombinant can appear more than the parental (for example, if the parental is lethal or by pure chance) but in this case I belive it is simply a different organization on the chromosomes


text:
What is the intracellular chloride concentration in rat T-cells or thymocytes
I'm modeling acid-base in T-cells as based on Grinstein J Gen Physiol 1984; 83: 341-369. I have an estimate of strong ion difference (SID), and Grinstein gives Na and K, but for SID to be true at 33 mM with K 147 mM and Na perhaps 20 mM Cl should be  (K + Na) - SID = 134 mM which is hard to believe but I could find no data on the subject.

Where is your estimate of SID from?

Felber and Brand 1982 estimate the intracellular T-cell chloride concentration to be about 30 mmol, which seems to me to be on the high end for intracellular chloride in mammalian cells (though my experience is mostly with neurons, I'm not as confident of intracellular chloride concentrations in other cell types; for a neuron I'd expect <10mmol). Still, that leaves a big anion gap for your SID estimate.
I think it is more likely that your SID estimate is simply wrong. The number you report sounds like an extracellular SID; Kowalchuk et al 1988 suggest intracellular SID is about 4X extracellular for muscle, which sounds about right for your situation as well.
Most of the intracellular anion contribution is provided by negatively charged proteins, amino acids, lactate, etc, rather than strong ions like chloride. Many of these are nearly completely deprotonated at physiological pH, though (for a typical amino acid the first pKa is ~2).

Felber, S. M., & Brand, M. D. (1982). Factors determining the plasma-membrane potential of lymphocytes. Biochemical Journal, 204(2), 577-585.
Kowalchuk, J. M., Heigenhauser, G. J., Lindinger, M. I., Sutton, J. R., & Jones, N. L. (1988). Factors influencing hydrogen ion concentration in muscle after intense exercise. Journal of Applied Physiology, 65(5), 2080-2089.

Thanks a lot - my estimate of SID was based on a buffer capacity of 25 mmol/l/pH as reported by Grinstein at pH 7 - for lack of other knowledge assuming a KA of 2e-7 like histidine gives from Van Slyke 1922 JBC equation 17 an estimate of ATOT , and from that using charge balance a value for SID.. But I can see you have to model the many negative charges on proteins in a different way. Thanks a lot for this help

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Why didn't more muscles evolve the endurance of heart muscle?
The heart is a muscle capable of both the quick contraction of white muscle cells, and also the endurance of red muscle cells. Why haven't more muscles in the body adapted the same combo of abilities? Is there a known weakness to the heart muscle? Excessive energy consumption, or something else?

Different strokes for different folks, as they used to say.

Our heart, diaphragm, and arterial muscles need to work 24/7. No other muscles even come close to that requirement, so they evolved in different ways. Always be wary of asking Why? when it comes to evolution.


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LAMP (isothermal amplification), hydroxy naphtol blue , disodium salt" or just hydroxy naphtol blue?
I am reproducing this work on LAMP (isothermal amplification)
Article A new visually improved and sensitive loop mediated isotherm...
,
but I am a bit confused  about the difference between "hydroxy naphtol blue", and "hydroxy naphtol blue , disodium salt". They hav a very huge difference in price. One is 470 USD and 40 USD for the same aliquote.  Or for LAMP there is no difference?
E.g. Price for HNB
https://www.sigmaaldrich.com/catalog/product/mm/104593?lang=de&region=CH&gclid=CjwKCAjw4rf6BRAvEiwAn2Q76quMK0jzJnsEL5Dsjh_rwYhGCz_Foj5ybiH4o8vNCZQ8S53qkaiA9RoCisIQAvD_BwE
and HNB disodium salt
https://www.sigmaaldrich.com/catalog/product/sial/219916?lang=de&region=CH

The sodium salt is the conjugate base of the raw compound, likely formed by reacting it with a strong base like Sodium Hydroxide. I'm curious what function it serves in the LAMP protocol. Can you cite the protocol? They might be capable of serving similar functions in solution, but they are not interchangeable in a reaction recipe, as one will lower the pH of an aqueous mixture more than the other. Probably a better question for https://chemistry.stackexchange.com

I just found a LAMP protocol which provided a CAS number corresponding to the Hydroxynaphtol Blue, not the sodium salt. Make sure to cross-check the methods section of the work you are trying to reproduce though.


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Will renal blood flow decrease in response to dehydration?
If dehydrated, does the correction of ECF osmolarity happen slowly enough for ECF (and therefore plasma) volume to be temporarily depleted and therefore reduce renal blood flow?
If dehydration is taken to mean ECF hyperosmolarity, would fluid not just move out of cells to restore normal osmolarity, without affecting ECF volume or renal blood flow?

Please spell out any abbreviations that are not widely used. Specifically, what does ECF mean?

Apologies: extracellular fluid.


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instances of virus transmission-enhancing research approvals
In February 2019 this article by epidemiologist Marc Lipsitch and professor Tom Inglesby raised concern about secret virus research.
Washington Post article link.

In 2014, U.S. officials imposed a moratorium on experiments to enhance
some of the world’s most lethal viruses by making them transmissible
by air, responding to widespread concerns that a lab accident could
spark a global pandemic. Most infectious-disease studies pose modest
safety risks, but given that these proposed experiments intended to
create a highly contagious flu virus that could spread among humans,
the government concluded the work should not go on until it could be
approved through a specially created, rigorous review process that
considered the dangers.
Apparently, the government has decided the research should now move
ahead. In the past year, the U.S. government quietly greenlighted
funding for two groups of researchers, one in the United States and
the other in the Netherlands, to conduct transmission-enhancing
experiments on the bird flu virus as they were originally proposed
before the moratorium. Amazingly, despite the potential public-health
consequences of such work, neither the approval nor the deliberations
or judgments that supported it were announced publicly. The government
confirmed them only when a reporter learned about them through
non-official channels.

Have there been other instances of transmission-enhancing research approvals since the apparent end of the moratorium?


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Why does this oxygen duration chart have increased times above 30,000 FT MSL?
This oxygen duration chart from an airplane shows the amount of time a pilot can be on oxygen at a specified altitude (in 1000s of feet).  For example, the chart shows two pilots able to cruise at a cabin altitude of 35,000 FT MSL for 182 minutes using a diluter demand system or 192 minutes using 100% oxygen.
I have one question.

Why does the oxygen duration chart show increasing times above 30,000 FT MSL?

“Why does using 100% oxygen provide greater time...” It does not, the bold numbers (for 100% oxygen) are all lower than the lighter face numbers - as explained at the bottom of the chart.

You're right.  I've updated the question.

I wonder if someone on the Physics stack would know. I can't think of a biological reason this would be the case, but maybe it has to do with the physical properties of the gas in the storage containers. Like, maybe at lower altitudes, more of the stored oxygen remain in the system because of the higher atmospheric pressure.

The bottle is regulated to output 75psi to all the passengers on the plane.  It could be the difference between PSIA and PSIG.  I'll ask them.  Thanks.

This might be worth asking on the aviation stack...

This is related to the diluter demand system, O2 present in the cabin, and tracheal pressure.

The diluter demand system is designed to compensate for the
short-comings of the continuous flow system. It   gives the user oxygen
on-demand (during inhalation) and stops the flow when the demand
ceases (during exhalation). This helps conserve oxygen. Additionally,
the incoming oxygen is diluted with cabin air and provides the proper percentage of oxygen, depending on the altitude. This system
is typically used at altitudes up to 40,000 feet.

Source: Oxygen Equipment: Use in General Aviation Operations - Federal Aviation Administration
When you get at altitudes higher than 35,000 feet you're more or less totally reliant on the oxygen provided by the diluter, that's why the diluter demand is very close to the cruise time. If there's low air pressure in the cabin above 35,000 feet there won't be enough oxygen for normal body function, and you run the risk of becoming hypoxic within half a minute.

Toe of Useful Consciousnees (TUC) per Effective Performance Time (EPT)

Look at the chart below:

Tracheal oxygen partial pressure starts at 149mm. Hg for sea level and can drop to 20 at 40,000 feet. If oxygen is given according to the % supplement O2 required for inspired air, the tracheal pressure stabilizes back to what it is at sea level. Above 30,000 feet, tracheal oxygen partial pressure cannot be maintained at 149mm. Hg. Therefore you need to use the diluter longer to at least maintain it close to 149mm. Hg. Or at level where the mm. Hg. isn't extremely low.
The required mean tracheal oxygen partial pressure can be different at the same altitude depending on the liters of O2 per minute BTPS (Body Temperature and Pressure Saturated) being inspired.
Source: Introduction to Aviation Physiology
Fore example, according to 14CFR 23.1443:

(ii) At cabin pressure altitudes above 18,500 feet up to and including
40,000 feet, a mean tracheal oxygen partial pressure of 83.8 mm. Hg
when breathing 30 liters per minute, BTPS, and with a tidal volume of
1,100 cc. with a constant time interval between respirations.
(2) For each flight crew member, the minimum mass flow may not be less
than the flow required to maintain, during inspiration, a mean
tracheal oxygen partial pressure of 149 mm. Hg when breathing 15
liters per minute, BTPS, and with a maximum tidal volume of 700 cc.
with a constant time interval between respirations.

So, at above 30,00 feet you will use most of the diluter demand oxygen to preserve tracheal pressure until the plane has stabilized. At lower altitudes the diluter demand is lower because you can reach safer altitudes faster.

Doesn't this mean you should use more oxygen above 30,000 FT MSL?

The % required O2 oxygen (inspired) needs to be 100%. That is because if you use the diluter system the air in the cabin is too thin to provide any meaningful O2. For the diluter system the incoming oxygen is diluted with cabin air and provides the proper percentage of oxygen. At 30,000 FT MSL oxygen in the air too thin and you're going to use more of O2 provided by the diluter.

Why then does the chart show in an increase in oxygen available time above 30,000 FT?

Oxygen in the air will be too little but the oxygen available from the diluter will increase above 30,000 FT. O2 is too thin at that level to maintain tracheal pressure and % saturated O2 in the blood the availability of O2 will increase. If you're flying at 35,000 for 182 minutes, you're going to need 182 minutes on diluter system and some extra so that the shift to lower altitudes minimizes the effects of altitude acclimatization.

I wonder if the physics stack had a different answer, or a better one. If they did and you could provide a link I would love to see what they answered with.

I don’t quite understand it all.  I’ll have to think about what you said.  Here is the link to the Physics question. https://physics.stackexchange.com/q/578377/274173.  I’ll probably ask in the aviation side too.

If you got time check the Introduction to Aviation Physiology I linked. It has extensive information which might help in elucidating some of your questions or confusions. It comes from the FAA.

Thanks.  I will do that.

Are you saying that since the tracheal pO2% is lower at 35,000 FT MSL (132 vs 149) we don't need as much O2?

Let us continue this discussion in chat.


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Looking to understand the difference between (Fibroblast Growth Factor) FGF-2 and FGF-5
Non-biologist nor medically trained person here, but still nonetheless interested in the functioning of the human body, and more specifically, hair growth cycles.
I've read in several sources that FGF-2 is potentially a hair growth 'stimulant' (source), whereas FGF-5 is a potential hair growth inhibitor (source) and I was looking to better understand the differences between the two?
According to a basic definition, and the bounds of my current knowledge, FGF's are signalling proteins that are involved in a whole host of bodily functions including but not limited to wound healing.
What are the potential differences between '2 and '5 that makes them appear to affect hair in opposite ways, as I would have thought that the general FGF family would act in a similar way if anything.

Growth factors and other signaling molecules are often grouped into families based on sequence and structural similarity, not necessarily by function. It's actually rather common to have this scenario, where one family member promotes an effect opposite that of another family member. All that means is they probably bind to their receptor(s) in a similar manner, with one being an agonist and the other an antagonist.

I'd suggest looking at this article on the FGF family. You will find a lot of information there about comparative analysis of the different proteins therein. For example (FGFR = FGF receptor, which binds FGF to transmit signals):

FGF–FGFR binding specificity is regulated both by primary sequence differences between the 18 FGFs and the 7 main FGFRs (FGFR1b, FGFR1c, FGFR2b, FGFR2c, FGFR3b, FGFR3c and FGFR4) and by temporal and spatial expression patterns of FGFs, FGFRs and HSGAGs. The alternative splice isoforms of FGFRs are generally tissue specific: the b isoform is usually expressed in epithelial tissue, whereas the c isoform is usually expressed in mesenchymal tissue23. Ligands are produced in either epithelial or mesenchymal tissue and generally activate receptors of the opposite tissue specificity: in normal physiology, a ligand produced in the epithelium will activate a mesenchymal receptor and vice versa. Several ligands, including FGF1 in particular, pose an exception to this general understanding by promiscuously binding to both b and c isoforms of certain FGFRs. Pathological states can result from a breakdown in binding specificity, as is common in cancers in which FGFs are overexpressed24. Structural studies of FGF1, FGF2, FGF8 and FGF10 with their cognate FGFRs show that sequence diversity at FGF N termini, variation in β1 strand length (FIG. 1b) and the alternatively spliced regions in D3 dictate their binding specificities (FIG. 2b, c).

So it's rather complex. Differences in FGF function are at least in part due to small biochemical differences that may give them differential affinity for different FGFRs, which then go on to transmit the FGF signals down the line. But at the same time the FGFs/FGFRs are expressed in different tissues, meaning that they may have relatively narrow spheres of influence.
If you look here you will see that different FGFs actually have relatively low similarity at the amino acid sequence level, and in some cases quite significant differences in gene structure (though they don't talk about 2 and 5 specifically). One notable difference there:

Most FGFs (FGFs 3-8, 10, 15, 17-19, and 21-23) have amino-terminal signal peptides and are readily secreted from cells. FGFs 9, 16 and 20 lack an obvious amino-terminal signal peptide but are nevertheless secreted [25,26,27]. FGF1 and FGF2 also lack signal sequences, but, unlike FGF9, are not secreted; they can, however, be found on the cell surface and within the extracellular matrix.

For some work on this topic specifically targeted towards FGF2 and FGF5, you can see this paper, which has this table about the location of FGF expression in follicle cells, showing that they are expressed in different places:

apologies to people with screen readers, I didn't have the motivation to copy it out into text. Here is a summary figure that they give:


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Why do we have to move in the cold for higher chance of survival?
To survive in the cold temperatures, a person should move as much as possible so that they do not freeze to death. But constantly moving also leads to the body becoming more and more exhausted.
Why doesn't the human body "know" that it is better to invest energy directly in heat rather than in movement and the resulting heat?
After all, the body already optimizes blood circulation, protecting the inner organs better than limbs like hands and feet.

Asking "why" about anything to do with evolution is tricky, because the only real answer is "they managed to survive and reproduce".  One might suggest that it has something to do with humans and their ancestors having lived mostly in tropical climates, so there was no great evolutionary pressure to develop adaptions to cold.  Peoples whose ancestors inhabited cold climates for many generations, like the Inuit or Tierra del Fuegans, DO have adaptations for cold tolerance.

It seems to me ironic that you talked about the body “knowing” (commendably in italics), when, in fact, the problem is solved by the fact that we do know — no italics, because it involves our brain. Shades of wanting Nature to reinvent the wheel, but make it square. I think she knows better.

Also note that the body DOES have a way to produce heat (within limits) without movement.  It's the shivering reflex: https://en.wikipedia.org/wiki/Shivering

Don't get me wrong. I believe that the human body and nature in general is a miracle and I admire it. I just ask to learn more about it.

@Dani: If you believe the human body is a miracle, you should migrate the question to the (religion of your choice) site.

As with any evolutionary "why" question, most any answer will likely involve some speculation. But we can still think about what we do know in relation to the question.
First, lets think about thermogenesis in humans. As your questions mentions, humans move to stay warm. This is because the conversion of chemical energy (in the form of ATP) into kinetic energy in our muscles is inefficient, resulting in some of the kinetic energy dissipating in the form of heat (instead of moving your body). Shivering is actually a cold-induced reflex that helps our body maximize the amount of chemical energy converted into heat through skeletal muscle contraction. So, in a sense, you body does "know" how to invest in generating heat without moving (without moving as much at least).
A different mode of non-shivering thermogenesis in mammals is mediated by a specialized type of fat called brown adipose tissue or brown fat. This brown fat is used by some animals to generate heat during periods of hibernation. However, adult humans tend to have very little of it. Human infants on the other hand, carry can carry quite a bit (up to 5% of total body weight). This could relate to a number of factors that make infants more sensitive to cold than adults, including having less developed skeletal muscles that are unable to generate much heat though movement or shivering.
It seems like one reason we can't generate heat very well without moving is that we don't carry much of this brown fat around. So, why don't we then? It could be that it's just energetically expensive, and those resources can be better spent elsewhere. Or maybe there could have been some negative health effect associated with carrying excess brown fat in adults. Whatever the reason, it comes down to a lack of selective pressure to maintain this extra tissue into adulthood.
But there's one other, more behavioral solution that might be worth consideration (although it's purely speculation at this point). In most naturally occurring scenarios where the body would be approaching a state of hypothermia, simply staying put and waiting for the temperature to change will seldom be your best chance for survival, even if you are doing burpees to stay warm. In order to ensure continued survival, one may need to actively change their condition of being in an environment that's too cold to maintain sufficient body heat. Humans are pretty good at changing their immediate circumstances. It might involve getting up and finding/building shelter, gathering fuel to make a fire, or migrating to someplace warmer. But in any case, it would require some amount movement accompanied by a cognitive motivation to move. Feeling less cold seems like a powerful motivator to me. If we had more robust means stationary thermogenesis, it's possible that we'd be able to survive a longer spell out in the cold just by conserving our energy a bit better, but that might not be the most effective survival strategy given the situation. Calories and liquid water can be hard to come by in extremely cold environments, and waiting for some other physiological need to motivate action might be less advantageous than proactively moving around to alter one's state of being too cold. Just a thought.

Actually, the body is able to warm itself by using uncouping protein 1 (UP1) and other physiological methods
The coupling in uncoupling is referred to the relation between the protein gradient and the synthesis of ATP (biological energy currency). UCP1 creates an alternative channel for the protons to pass. This protons have energy that, when not used to create ATP, will dissipate as heat
But every process has it's limitations. By moving you are forcing your body, in addition, to transform chemical energy to kinetic energy and that kinetic energy will transform to heat
Speculation
The movement will pump blood to the limbs and transfer the heat created by UCP1 from the inner cells to the outer cells, heating you up and allowing more UCP1 to be created in the inner cells and to use more energy for heating up.
This is a speculation because:

I don't know and didn't found an article examining what regulates the levels of transcription and translation of UCP1
I don't know if UCP1 are created in all cells or only in the outer ones


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What is this giant mosquito-like insect?
I found this bug in my kitchen in this morning, in a suburb of Houston Texas, about 30 miles Northwest of downtown. It was on the wall, and when I went in for a closer look, it quickly flew away - up towards the light, then crash landed behind the refrigerator where I hit it with bug spray.
It looks sort of like a mosquito, but much much larger.
Everything I find online about "giant mosquitoes" points to the Crane fly or "mosquito hawk" - which I've seen plenty of (very common here). I'm no expert, but this doesn't look like a cranefly.
I also read that giant mosquitoes are known to hatch after hurricanes, and there was just a huge one <200 miles from me. But those accounts speak of smaller insects (albeit, still very large for a mosquito).
For example, this article about "gallinippers" in North Carolina, speaks of mosquitoes only the size of a penny.
I did not think to put a coin in the shot for reference, but based on the size of the paper towel underneath it, it must be at least the size of a quarter.
Is this even related to a mosquito? What could it be?

The better entymologists among us may need to correct me, but I believe you are looking at a robber fly, especially based on the characteristic long, tapering abdomen, as well as the proboscis that reminded you of a mosquito and the large size.
I see a couple people posting images from Texas that look a bit like yours (especially the all-black body) on Google images but none of these mention a genus/species for me to dig further on. Bromley, S. W. (1934). The robber flies of Texas (Diptera, Asilidae). Annals of the Entomological Society of America, 27(1), 74-113. may be useful but is a bit too deep for me to dig into for you.

iNaturalist has over 9000 user-submitted photos of robber flies (family Asilidae) from Texas alone, breaking down into 9 sub-families, (I don't know how many genera) and further into 96 species. Here is the breakdown into 9 subfamilies ... I can't tell which one it belongs to: https://inaturalist.ca/taxa/47982-Asilidae/browse_photos?grouping=taxon_id&place_id=18

Bromley 1934 is also available here; the advantage to this copy is it's free of charge, but printing (if desired) is one-page-at-a-time.  Other disadvantages include the age of the work (it is almost certain that more species are presently known from Texas), the need for specialist vocabulary, and the paucity of illustrations.


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Why does vacuum sealing of foods prevent spoilage from anaerobic bacteria?
I have noted that many purchased food items in containers only require refrigeration after they have been opened, thus eliminating the vacuum seal.  Air contains bacteria and fungus spores that enter the food container and if not refrigerated, the aerobic micro-organisms will proliferate, thus altering and rotting the food.  The air also allows any dormant micro-organisms that survived the factory sterilization process already in the food to come back to life and proliferate.
However I do not understand why anaerobic bacteria, that don't require and cannot survive in air, do not proliferate and thrive in the vacuum sealed food containers.  That plus the fact that we can leave already opened food items such as honey, jams, and peanut butter out of the refrigerator for weeks but they do not spoil.

I'm betting most of those foods are sterilized with heat either before or after being sealed in their packaging, similar to how you would can foods at home, just on an industrial scale. The vacuum seal functions to prevent microbial contamination of a sterile product, not just to prevent aerobic organisms from growing.

Honey, jams, and peanut butter each have antimicrobial properties on their own that help delay or prevent spoilage.

I think honey, jams, peanut butter antimicrobial properties isn't directly what prevents or helps with avoiding spoilage. It is their water activity being quite low. The water activity of peanut butter is typically 0.35, which inhibits the growth of spoilage and pathogenic microorganisms.

Just adding a little bit more info taking from the answer above.
You got two types of anaerobes:

Facultative anaerobe that makes ATP by aerobic respiration if oxygen is present. It can switch to fermentation or anaerobic respiration if oxygen is absent. Most common example of a food pathogen in this category: E. coli

Obligate anaerobe which are killed by normal atmospheric concentrations of oxygen. Example: C. botulinum, which is mentioned in the answer above.

I am using C. botulinum as the example here because it is widely used in making HACCP (Hazard Analysis Critical Control Point) plans. These are plans with certain steps which make sure that what you're producing is proven safe for consumption.
Now, C. botulinum vegetative cells die in the presence of oxygen. The spores allow the organism to survive when there's lack of nutrients and/or oxygen levels are too high. The spores are also heat-resistant. C. botulinum cannot grow below a pH of 4.6, so acidic foods, such as most fruits, tomatoes, and pickles, can be safely processed in a water bath canner.
If the pH is above 4.6 there's usually a CCP (Critical Control Point) in the HACCP plan to make sure the product is pasteurized. For C. botulinum that is a kill step at 85°C for 5min minimum to destroy the toxin.
Another product example would be cold brew coffee. You need a certain % of dissolved O2 so that C. botulinum doesn't proliferate since cold brew coffee has a high pH (>4.6 usually).
Another problem with Reduced Oxygen Packaging (ROP), not related to anaerobic bacteria, is mold growth. To mitigate this some products might have the air present in the bag replaced with nitrogen then flushed. Nitrogen Flushes in ROP can reduce the rate at which mold can grow.
TL;DR: They do grow but there's certain steps each company needs to take to prove safety of their product before sale. If your HACCP plan accounts for C. botulinum you're sure to knock out a wide majority of obligate anaerobes (if not all) that could grow in your product.

I do not understand why anaerobic bacteria, that don't require and cannot survive in air, do not proliferate and thrive in the vacuum sealed food containers

They do. Vacuum sealing can prevent aerobic bacterial growth but does not prevent anaerobic growth.
Botulism is a particularly dangerous consequence. If food containing C. botulinum spores is sealed without being properly treated (usually by heating) or otherwise by being inhospitable to bacterial growth (often due to acidity or salt), dangerous botulinum toxin can accumulate and be dangerous or fatal when the food is later eaten.


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Why do dragonflies have these special little spots on their wings?
The wings of several kinds of dragonflies I've seen here in Taiwan all have an apparently special little pigmented spot near the ends of each wing.
Does this spot have a name and a function?
below x2: Taken today in Hsinchu county, Taiwan. Note arrows. I've also asked Identify these two large dragonflies in Taiwan?
Click for full size

below left: from Identify this black dragonfly with bluish coloration along its flat top, yellow on it's mid-body and green on its head below right: from Identify this black dragonfly with a bright bluish-white band around its body
Click for full size

Pterostigma is what those spots are. Wikipedia article is at https://en.wikipedia.org/wiki/Pterostigma.
I read the summary of the technical article below.
The pterostigma are heavier than the rest if the wing, and so the insect can glide faster without a destabilising flutter beginning.
The author also believes that the pterostigma contribute to more efficient active flight.
Technical details at:
Norberg, R. Åke. "The pterostigma of insect wings an inertial regulator of wing pitch". Journal of Comparative Physiology A. 81 (1): 9–22.
doi:10.1007/BF00693547.

This is excellent, thank you very much! btw I've just asked Why this inertial regulator of dragonfly wing pitch reduces self-excited coupled flapping and feathering vibrations and improves gliding flight speed in Aviation SE. I am not sure yet if it will "fly" there or not, but let's see what happens.

That question "flew" as did this one. Thanks for your answer!


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Identify these two large, colorful dragonflies in Taiwan?
Here are two dragonflies that I photographed today in Hsinchu county Taiwan. They are both quite large, with a body length of about 5 or 6 cm.
I often see them in the same pond or nearby marshy area. They seem pretty confident and are easy to photograph as long as you don't make a big commotion.
The arrows were drawn for my other question Why do dragonflies have these special little spots on their wings?
Is it possible to identify these two species? I can break them out as separate questions if necessary; I don't want to flood the site with "identify this dragonfly" questions.
The first is jet-black everywhere except for a robins-egg blue powdery coloration along the top side of the first two-thirds of it's abdomen. It's wings, like most but not all dragonflies, are transparent.
The second has some amount of red almost everywhere; its eyes and thorax are dull red and it has bright red patches on each segment of its abdomen. Notably its wings are solid opaque red, except for the furthers 1 cm which is transparent. The tiny "special spots" on the tips of each wing are a particularly bright shade of red!

one more: Identify this dragonfly with orange body and orange wings?

Looks like this species is Orthetrum triangulare commonly known as blue-tailed forest hawk. It is an Asian fresh water dragon fly species.
As you mentioned that the dragonfly had a bluish hue, it became clear.

The other one looks like Neurothemis ramburri, commonly known as red perch Reference

Neurothemis is a genus of dragonflies in the family Libellulidae. Most Neurothemis species are red in color.
Neurothemis ramburii (Brauer, 1866) is distributed from Sundaland to New Guinea. There are records from Peninsular Malaysia, Taiwan, the Andaman Islands, Sumatra, Java, Borneo (Sarawak, Sabah, Brunei and Kalimantan), the lesser Sunda islands, the Philippines, the Bismarck islands and New Guinea. It is a widely distributed and common species that thrives in disturbed habitats.

Wow that was fast, thank you!

@uhoh you may accept the answer if you are satisfied for the future references

indeed, thank you for the reminder. I generally wait a week or more to allow for review by other readers and the posting of additional answers, and a week has now passed.


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Identify this dragonfly with orange body and orange wings?
The photo shows a red dragonfly on top (in front of some hot pink snail eggs) but an orange dragonfly with orange and perhaps translucent(?) wings near the bottom. This is the best resolution I could get. While the red one is easy to photograph (see Identify these two big, beautiful dragonflies in Taiwan?) this orange species is really jittery and difficult to approach.
I believe I have seen dozens of them in an isolated grassy patch in a parking lot, but they never landed and I could not capture a photo or see them clearly, but today this one was "available" for a photoshoot.
The orange dragonfly's body is about 4 to 5 cm long, the location is Hsinchu county Taiwan. That's all I've got, except that the last centimeter or so of the wings appear to be almost transparent.

These seem to both be Neurothemis taiwanensis.
On iNaturalist, if you search for dragonflies in Taiwan, it finds 104 species observed and submitted, and this Neurothemis taiwanensis is the most popularly-submitted species.
Browsing the gallery of photos in their database shows both red and orange varieties. If we filter the sex on just males, we see mainly deep-red ones:

...and filtering on just females yields mainly orange ones but also some red ones:
https://inaturalist.ca/taxa/503081-Neurothemis-taiwanensis/browse_photos?term_id=9&term_value_id=10&place_id=7887

Wow! Very nice, Yes I see that now. Okay I will now try to figure out how to use the inaturalist.ca site's features. Thank you very much!


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Are coronaviruses gaining an evolutionary advantage?
So there are 7 known strains of coronavirus that are known to infect humans: 4 that cause the common cold (229E, NL63, OC43 and HKU1), and 3 that have been known to cause acute respiratory infection (SARS, MERS and now COVID-19). They're all beta-coronaviruses except for 229E and NL63.
I can't help but notice the latter 3, which also happen to be the most serious, have all emerged very recently and within less than a decade apart from one another. I tried to find out how long the common cold strains have been around for, but can't find too much information on that (I found one article from science daily that says the common cold could have originated in birds around 200 years ago, but that's about it).
Does anyone have more information on this? Is the fact that SARS, MERS and COVID-19 emerged so close to one another a trend or just a coincidence? Are there any notable scientists who've noticed this and have an explanation as to why?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Note, your question is unclear and the title and body of your question don't seem to match. Please only ask one question at a time to improve the chances that you will get answers and makes them more accessible for future users. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Thanks for your response! I just graduated from undergraduate school so my biology skills aren't incredible yet so forgive me if my question seems vague and non-specific. I kind of  just dumped whatever information I knew in the description. So the purpose of the question was just to figure out if there was a reason why coronavirus diseases specifically keep popping up. The reason why I mentioned the common cold strains was because I was wondering if there's evidence that they emerged in the human population recently, too.

It is not a coincidence, but it doesn't have to do with sudden evolutionary changes, rather with human behavior.
The three viruses you mention are zoonotic — they can infect different species, including humans.
Increased development of formerly untouched lands is bringing people into contact with animals (and existing, but formerly unknown zoonotic pathogens) in greater numbers.
Humans bring the virus back to concentrated human populations — cities, say — either being infected themselves, or bringing back infected animals for consumption. This increases the opportunities for further spread.
With the help of global leadership that is corrupt, incompetent, or antiscience, the multiplier effect of repeated infections in cities turns a small pool of cases into a pandemic. Rinse and repeat.

The risk of emerging infectious diseases such as COVID-19 from animals is on the rise, in large part because of our environmental footprint and the blurring between the natural and the built environments. Increasingly, humans, livestock and wildlife are interacting in new and unexpected ways, bringing new species – and their resident infections – together with unpredictable results.
Climate change is accelerating the loss of animal habitats and the ways humans change the land. Cutting down old-growth and rain forests, which harbour a rich biodiversity of life, to create agricultural or pastoral land potentially brings people and livestock in closer contact with previously isolated populations of bats, and other animals harbouring previously unencountered disease. In turn, biodiversity loss threatens natural food sources which means animals seek other sources of food found where people live. As climate change causes large disasters like floods and drought, human food sources are also lost, and growing food insecurity pushes people to further encroach on animal habitats, increasing animal contact and contributing to the trade in wildlife.
The speed and magnitude of environmental change has implications for future epidemics and pandemics. The first few cases of COVID-19 have been traced back to a ‘wet market’ that contained wild animals sold for food or medicines. Such markets can be ideal environments for zoonotic spread as the unusual mixing of animals (which is not common in the wild) can provide opportunities for viruses to jump between species, and potentially then to people.

Development isn't just loosing coronavirus — there are other pathogens that have been loosed by encroaching on their natural reservoirs:

We invade tropical forests and other wild landscapes, which harbor so many species of animals and plants — and within those creatures, so many unknown viruses. We cut the trees; we kill the animals or cage them and send them to markets. We disrupt ecosystems, and we shake viruses loose from their natural hosts. When that happens, they need a new host. Often, we are it.
The list of such viruses emerging into humans sounds like a grim drumbeat: Machupo, Bolivia, 1961; Marburg, Germany, 1967; Ebola, Zaire and Sudan, 1976; H.I.V., recognized in New York and California, 1981; a form of Hanta (now known as Sin Nombre), southwestern United States, 1993; Hendra, Australia, 1994; bird flu, Hong Kong, 1997; Nipah, Malaysia, 1998; West Nile, New York, 1999; SARS, China, 2002-3; MERS, Saudi Arabia, 2012; Ebola again, West Africa, 2014. And that’s just a selection. Now we have nCoV-2019, the latest thump on the drum.

The three viruses you mention are serious. MERS and SARS have high fatality rates. The third (SARS-CoV-2) is highly contagious. These attributes disrupt everyday life.
But the aforementioned and other viruses are also serious for similar reasons. Zika, for instance, can cause life-altering birth defects, has been known about for decades, and human-caused climate change has been enabling it to spread to more densely-populated areas.
Evolution — natural selection — takes place over thousands to millions of years. Human behavior has changed the earth only within a few hundred years, much of it in the last century or so.

Thanks for your response. I was definitely thinking that disruptions in the ecosystem such as climate change, deforestation and increased interaction with animals played a role like you said. Maybe my question wasn't clear enough, but I was focused specifically on if there was a reason why outbreaks caused specifically by coronaviruses have been happening in recent history. I appreciate your detailed response.

There are a number of recent outbreaks caused specifically by other types of viruses, as well. But the answer to your question is no, zoonotic viruses are not becoming more prevalent due to evolution.


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QA/monitoring in recombinant vaccine manufacturing
On a16z[0] podcast on vaccines[1], an interesting tidbit came up: vaccine manufacturing in cell cultures is expected to hit a major challenge in terms of quality control due to unpredictable behaviour of cells.
The issue was mentioned only in passing during the podcast, specifically Rajeev Venkayya[2] said:

First of all, we need to see if these vaccines can be scaled up from a manufacturing standpoint very, very quickly. And not just be produced at scale but also produced with a reproducible high quality.
This is one of the biggest challenges that you run into when making biologics at large scale, particularly when we're talking about hundreds of millions or even billions of doses.

I'm wondering how monitoring and quality assurance looks for cell cultures in an industrial setting. What are practical examples of what can go wrong with a cell culture that affect the final output (e.g. a vaccine) and how does one detect these issues? Is cytometry involved for "cell interrogation" or some more specialized methods are used?
I tried researching this question on my own, but quick googling didn't yield much. I'm a software engineer with deep learning experience, I look at this issue from a computer vision point of view and wonder if anything my field could do to contribute to solving this issue.
[0] a VC firm with a science leaning
[1] which is very good! https://a16z.com/2020/08/14/vaccines-vaccinology-renaissance-covid-pandemic-beyond/
[2] board member of Coalition for Epidemic Preparedness Innovations

Can you clarify what you mean by "observability" for cell cultures? It would help if you expanded a bit on the relevant points raised by the podcast, as it's an hour long and questions on SE sites should be self-contained.

Thanks for the comment! Unfortunately, this specific issue has been mentioned in passing so not much more detail is available to me but let me try to clarify the question. Specifically the use of "observability".

@MattDMo expanded my question. let me know if that helps!


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Are bryophyte sporangia multicellular?
My research on the matter can be summarized in a sentence: "It [sporangium] can be composed of a single cell or can be multicellular" (Source: https://en.wikipedia.org/wiki/Sporangium). Yet there shouldn't be a reply placed between "They are" and "They aren't" test options, speaking of "Are bryophyte sporangia multicellular?". A link to the source where I could ascertain whether the bryophyte sporangia is multicellular (if I could ascertain) is highly appreciated.

In Embryophyta (land plants), including bryophytes, the sporangium is usually a multicellular structure.

Perhaps you meant to ask about the number of spore mother cells (SMCs) in each sporangium? That varies across groups. In bryophytes, each sporangium has many SMCs, and accordingly produces a large number of spores. (Contrast this with angiosperms, where a megasporangium [called an ovule] has only one megaspore mother cell.)

References and further reading:

https://courses.lumenlearning.com/boundless-biology/chapter/bryophytes/

https://www.britannica.com/science/plant-development

Image attribution:
By LadyofHats. (Public domain;
https://commons.wikimedia.org/wiki/File:Hornwort_structures.jpg)

Thanks! Referring also to the "Great Soviet Encyclopedia" 3rd edition (1970-1979), in particular, a sporangium is multicellular in higher plants. Now, scarcely do I understand why a sporangium of angiosperms is multicellular if it has a single megaspore mother cell. Is this because of four megaspores - the daughter cells in the process of meiosis in a megaspore mother cell?

@Lesya It is multicellular because it has cells OTHER THAN the megaspore mother cell (and its derivatives): namely the nucellus. See https://botit.botany.wisc.edu/botany_130/diversity/plants/Vascular_Plants/Magnoliophyta/Angiosperms/ovule-labelled.html.


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Is this a young roach?
Looks like a roach to me, but dont know for sure or what kind. Measures about 2cm large. Location: central Mexico

short answer is that yes, it is a roach


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Why bovine serum albumin is used in mass-spectroscopy and how to interpret such data?
In the paper Network organization of the huntingtin proteomic interactome in mammalian brain, there is a description of a mass spectroscopy experiment where Bovine Serum Albumin (BSA) is added to a sample lysate and the same lysate without BSA was used as the control. I have a working knowledge of how mass spectroscopy works but I could not understand why BSA is used in this experiment. Can anyone help me?
This is probably a very trivial question. Excuse my ignorance, I am not a biology major. I tried google search to get an explanation for this but I didn't find anything satisfactory.

Their LC-MS-MS data was only semi-quantitative as gathered, meaning they could compare relative levels of one protein to another in the same sample, but not necessarily between different samples with a high degree of confidence. So, they spiked known amounts of BSA, an extremely well-characterized protein frequently used in the lab, into their samples and created a standard curve across different concentrations that correlated pretty well with the input amounts. They could then use this curve to better quantify the other proteins in their samples among all the different sample types. This in turn allowed them to say with greater certainty that, for example, Protein X was expressed at three-fold higher levels in Sample A than in Sample B. Otherwise, they would only have been able to say that Sample A expression of Protein X was higher than Sample B.

Hi Matt, Thank you very much for the answer. Your explanation sounds reasonable to me. Thanks again!

@incrediblesulk You're welcome. BSA is an extremely common reagent in biochemistry/molecular biology/cell biology labs, as it's useful for all sorts of things, including as a standard in many concentration measurements.


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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?


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Characteristics of Araneus hui (an orb-weaving spider)
What are the characteristics of Araneus hui? Neither thematic literature nor photos was found.
Mentioned in RU Wikipedia, reference wasn't found.
https://ru.wikipedia.org/wiki/%D0%9A%D1%80%D0%B5%D1%81%D1%82%D0%BE%D0%B2%D0%B8%D0%BA%D0%B8

I found a number of images via Google Image Search

@MattDMo none of those photos in your Google Image search were A.hui (at least in the first few hundred) There were all Araneus diadematus or A.clerk or other common Araneus species.

@Noah It would help to know what characteristics you might be looking for, and maybe a 'why' would help. We don't know if you are interested in, say, the what colour they mainly have, or whether it is has genetic similarity to another species, or its evolutionary phylogeny, or something else.

@JimN I apologize for not specifying in advance. The initial interest was precisely in the appearance, including it's color. That is why I initially tried to find photographs.

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These pages cite papers that mention A.hui:
https://www.gbif.org/species/2160156
https://wsc.nmbe.ch/species/2910/Araneus_hui
The World Spider Catalog (WSC) offers papers to their users for free, and it is a free registration.
Browsing through the second pdf on the WSC, here is a sketch of the dorsal (top) view of the species:

The paper is primarily written in a language I cannot read.
The specific paper (book?) is:
Hu, J. L. (2001). Spiders in Qinghai-Tibet Plateau of China. Henan Science and Technology Publishing House, 658 pp.
658 pages is quite volumnous. The title of the paper suggests we limit our search to Tibet. Searching for Araneus images on iNaturalist in Tibet, there is a picture of one Araneus that has not been identified to species level, but it resembles the abdominal shape as in the drawing in the paper:
https://inaturalist.ca/observations/51273647
But the abdominal markings do not match at all. If you expand the geographical bounding box of the search around Tibet, you can browse a gallery of hundreds of possible pictures.

If anyone can translate the chinese characters in the 1. 2. 3. points in the footnote of the image, that would be great!

Female back view .  2. external female organ  3.  external female organ dissection

@PolypipeWrangler Great, thanks!


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Estimates of historical human population size
What are the estimates of minimum historical human population size, and how are they obtained from the current human genetic diversity?
I seem to recall a Scientific American article from over 30 years ago claiming a figure of 500-1000, but I can’t find any estimate now.

What exactly is your question?

I have modified your question slightly to make it more acceptable. If it is not what you meant do change it. It would be helpful to know precisely what you mean by "historical" — is it the pre-emergence from Africa I have assumed in my answer? Also, as a new user, please finish reading the [tour] which has information about using this site.

Although I cannot find the Scientific American article to which the poster refers, I assume that the “historic human population size” is the size of the human population in Africa before it underwent the expansion that accompanied the emergence from the African continent. Some important papers on this subject were published in the late 1990s (somewhat later than 30 years ago) and there is a suggestion in one of earlier estimates that I have not yet found a reference for.

There is an implication in the Harpending et al. paper (below) of earlier estimates of the order of 1,000. I will try to find the source (help on this welcomed).

Harpending et al. published a paper in PNAS of February 1998 in which they conclude an effective population size of the order of 10,000 individuals for most of the Pleistocene.

Reich and Goldstein published a paper in PNAS of July 1998 in which they conclude a maximum pre-expansion population size of 5,900.

A more recent study by Huff et al. published in PNAS in February 2010in which they estimated that the effective population size of human ancestors living before 1.2 million years ago was 18,500, and in which they rejected all models where the ancient effective population size was larger than 26,000

Why should the later estimate be more likely than the earlier ones?
Although the details of the calculations are complex (or at least too complex for me), it appears that the genetic markers that are used are crucial, and that it is important to have markers that represent rare mutational events. The earliest studies apparently used mitochondrial genes and the non-combining parts of the Y chromosome as markers. (These are used and are valid for studies of more recent time.) The limitations in these resulted in a shift to Alu repeats and microsatellites in the two 1998 papers, respectively. The 2010 paper used the insertion of the longer LINE repeats, which occur about one tenth as often as Alu insertions.
There is a Wikipedia article on this topic that may be also be of interest.


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What is this tiny creature?
Is this a bed bug or book lice? They were crawling all around the furniture.
Found in North East Florida, USA.

Is that a wooden surface? It could also be a termite. Do you have any additional pics?

Yes it was wooden surface. They were really tiny and fast. The other pictures are kind off blurry,

Book lice in Florida: https://inaturalist.ca/observations?place_id=21&subview=grid&taxon_id=372873
Bed Bugs in Florida: https://inaturalist.ca/observations?place_id=21&subview=grid&taxon_id=53667
Termites in Florida: https://inaturalist.ca/observations?place_id=21&subview=grid&taxon_id=118903&view=species
Ghost Ants in Florida: https://inaturalist.ca/observations?place_id=21&subview=grid&taxon_id=69122

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The picture is hard to see details, but it seems you might be dealing with ghost ants:

I'm guessing ghost ants over lice or termites or bed bugs because their light-coloured abdomen ends off in a pointed end, rather than a round bulbous end. The darker thorax and antenna are also a match. And the distribution/range of ghost ants seems to be heavily concentrated in Florida:

(Map source:
https://inaturalist.ca/observations?nelat=39.32226574471&nelng=-51.18647084246517&place_id=any&swlat=18.339761895743152&swlng=-117.94819281111599&taxon_id=69122 )
Apparently, they smell like rotten coconuts when crushed. (http://entnemdept.ufl.edu/creatures/urban/ants/ghost_ant.htm )
They eat any kind of food, and they are easily controlled by eliminating food sources (so if they are in your furniture, maybe look within cushions or cracks for old dried food and clean it out).


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Giving a sign to Pressure Potential, Osmotic Potential And Other Similar Quantities
When these quantities are mentioned with what reference do we give signs to them?
Why is Osmotic Pressure positive, but Osmotic Potential, negative?
What about Turgor Pressure (Pressure exerted by the protoplasmic fluid on the cell wall) and the Wall Pressure (Pressure exerted by the Wall as a reaction to the Turgor Pressure), what signs do we assign to them?
What I understand is that it's based on the tendency of water to enter or exit the system being studied, but I lack clarity on how signs are being assigned to these different quantities. When we talk about soil having a low, does low mean more negative or does it mean a lower magnitude osmotic potential, for example?

I think you already know the sign convention in calculating the water potential: the addition of solutes lowers the potential (negative vector), while an increase in pressure increases the potential (positive vector).(Another way of saying the same would be more solute = more negative.) {1} This is the same everywhere.

Pressure potential: The pressure potential in a plant cell is usually positive. In plasmolysed cells, pressure potential is almost zero. Negative pressure potentials occur when water is pulled through an open system such as a plant xylem vessel.{1} This means that it is negative during a "suction" action, otherwise, it is positive.

Osmotic potential (solute potential): The relationship of solute concentration (in molarity) to solute potential is given by the Van't Hoff equation:
Ψπ=−MiRTΨπ=−MiRT

(The formula, note, has a -ve sign.)
For example, when a solute is dissolved in water, water molecules are less likely to diffuse away via osmosis than when there is no solute. A solution will have a lower and hence more negative water potential than that of pure water. Furthermore, the more solute molecules present, the more negative the solute potential is.

Turgor pressure and wall pressure: I recommend reading this for a clearer understanding.

...This actual pressure which develops within such a cell is called turgor
pressure. This term can be applied with equal appropriateness to the actual
pressures developing in purely physical osmotic systems such, for example, as a
sucrose solution enclosed within a collodion or cellophane membrane and immersed
in water. As will become clear in the following discussion, TPs in osmotic systems
can sometimes be negative in value.

When the TP
is negative, that is, when the cell sap is under tension (see later), the WP is
likewise negative, the wall being subjected to a centripetal pull because of its
adhesion to the protoplasmic layer and cell sap mass within the cell.

On the basis of fundamental physical principles it is generally considered
that the WP and TP of a cell are equal in magnitude and oppositely directed.
This situation is not difficult to visualize for a cell in an equilibrium condition.
For dynamic states in which water is being gained or lost by a cell, however,
the validity of this assumption has been questioned.

{1}-https://en.wikipedia.org/wiki/Water_potential


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What's superposition and thread in RosettaCM?
I'm a beginner in structural biology.
I had a question while reading a paper on RosettaCM.
What does RosettaCM's superposition and thread mean?
I googled it.
As a result, the following results were obtained.

The term structural superposition refers to rotations and translations performed on one molecular structure to make it match another structure or structures. Inherent in the definition of structural superposition is an assumed measure of structural similarity. The optimal superposition is the one in which this similarity measure is maximized. Alternatively, one can define superposition in terms of a difference measure, such as root-mean square deviation ( RMSD ). In this case, the optimal superpositon is one in which the RMSD is minimized. The program ASH uses the former approach with similarity defined by the NER score.
Also, implied in any superpositon is an alignment, or mapping, between points in one structure (usually atoms) and those in another. Sometimes alignment and superpositon are used interchangeably.

Is this correct?
I also think of threads as part of a protein segment, is this correct?
In other words, in Rosetta CM's 1-step Global Superpotion, after aligning, the templates are stochastically determined, and the unselected templates are superposed so that RSMD is smallest.
Furthermore, the superposed template is a thread.
Is the above correct?

I’m voting to close this question because it is not about a biological process or mechanism.

Threading:
Start with a homologous protein. This protein can be thought of as two parts: (1) a backbone conformation and (2) a sequence of amino acids attached to the backbone. Threading occurs when you switch out the amino acids to those of your protein with unknown structure, but do not change the backbone conformation.
I believe the origin of the term is like beads on a string. The "string" does not change (the backbone geometry stays the same) but new "beads" (amino acids) are threaded onto certain positions.
The definition of superposition you found online is the correct definition for RosettaCM.

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What is this strange sea creature we found on the beach?
We found this on a beach in North Devon, UK. I've never seen anything like it.
There's a yellowy-ball in the middle with 5 pointed shells attached to it, each of which seems to have a single "leg" coming out of the bottom. It almost looks like it's 5 separate creatures feeding on something, but they're pretty firmly attached. Perhaps it's some sort of egg-sac that they're growing from?
Does anyone know what this is?

You have a Dosima: Also known as a Buoy Barnacle. A gallery of observations of these can be found here:
https://inaturalist.ca/taxa/462188-Dosima/browse_photos
They are found in the coastal UK and Spain area, New Zealand, and east and west N.America:

(source: iNaturalist observations)
These barnacles attach themselves to things that float, and if they don't have access to one, they will grow one themselves. Your image looks like five individuals attached to a central float that one of them (or a dead relative) constructed.

Wow these things are fascinating!


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When someone gets infected with influenza, and gains some immunity, is that immunity just as good as getting it from a vaccine?
A friend thinks that being infected with a new influenza virus means that little immunity is gained, unless you get a vaccine. But, he is forgetting that new strains can make current vaccines out-dated.
I'm sure the immune system will "remember" that particular strain just as well as getting a vaccine.
When someone gets infected with the influenza, and gains some immunity, is that immunity just as good as getting it from a vaccine?

Hi and welcome SE isn't for settling arguments. However, generally speaking - yes.

@Andrew Perhaps I can get information, statistics or something that could convince him.

@Andrew there's no reason that someone couldn't come here with a valid question to settle an argument or debate, it happens all the time. That's what factual knowledge is for, to dispel inaccuracies.

Not really answerable, unless you define what you mean by "just as good".  If you get immunity to (a particular strain of) the influenza virus via a vaccine, you don't have to experience having the flu.  If you get it from having the flu, you do.  IMHO that makes the vaccine better :-)

@MattDMo Okay - but I've received that criticism before.

@Andrew It's all about the subject matter and the way the question is posed. If a debate is purely opinion-based, too broad, or otherwise not on topic for the particular site, then it should be closed as such. If it is on topic, like this one, it should be accepted. IMO, whether or not there's a debate or argument at the root of the question is irrelevant. You shouldn't have been criticized for that.

Yes, infection-acquired immunity is (generally speaking†) just as good as, if not better than, getting vaccinated. Remember, the whole point of a vaccine is to simulate an infection and stimulate immunity without having to suffer through the actual symptoms of a real infection, potentially getting very sick or even dying. This is regardless of whether it's a "new" strain of virus or not.
† Not all exposures lead to good immunity, whether via infection or vaccination. Many times this can be related to immunosuppression or other immune system defects, but age and other factors like co-morbidities can also play roles as well.

For your addendum, the same can be said for some exposures that produce minor illness even when the immune system is functioning well.

Natural infections almost always yield a better immunity than that acquired through vaccination. However, vaccines yield a better immune-response than getting infected with influenza. That is so to say the side effects.
I want to backtrack to part of your questions where you say I'm sure the immune system will "remember" that particular strain just as well as getting a vaccine. and add a little bit of interesting information regarding influenza.
Some Influenza (A) stereotypes that infect humans are: H1N1, H2N2, H5N1, etc...
The H stands for Hemagglutinin and N is Neuraminidase. These are important in vaccine development. The H and N are proteins located on the surface of the virus and allow for entry into a cell for infection.
Strains are classified according to their hemagluttinins and neuraminidases. Every year when the vaccine for the seasonal flu is developed we don't know with 100% certainty which strain might be the most prevalent. Rather, surveillance data is used in deciding which flu might be the most prevalent. More info on the CDC Website.
So back to the question:

Does the immune system remember that particular strain just as well as
getting a vaccine?

Yes it does and there's a paper in PNAS that looked at something similar. This is related to something called “Immunological Honeymoon”. A theory that the first infection during childhood provides stronger immunological memory than a later infection.

The paper found that people who were 28 year old were more susceptible to the Spanish Flu (H1N1) in 1918 because they had been exposed to the wrong virus as children.
The elderly, however, had been exposed to H1N1 as children and were well protected. People who were middle aged or in their teens in 1918 had been exposed to H1N8 as children and were partially protected.
This I recon is just as good as vaccine, but more to show that the immunity acquired through infection is, in fact, remembered. For how long? That's a totally different question that varies from infection to infection. Some are life-long (such as measles), other are short lived requiring re-infection, or booster shoots in case of vaccination.


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Mystery rodent in Winnipeg
I spotted this rodent in Winnipeg, Manitoba, Canada on September 6, 2020.
It is about 10 inches long.

What is it?

That is a Franklin's Ground Squirrel

Winnipeg is part of its range:

Have a look at a gallery of such photos here: https://inaturalist.ca/taxa/179937-Poliocitellus-franklinii/browse_photos