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Can mRNA vaccine have flaws and generate the wrong spike protein?
Someone asked me if SARS-COV2 mRNA vaccine could create the wrong spike protein and have a negative effect on our immune system. Since I know too little about biology I couldn't answer that and started doing some deeper research than I did before on mRNA. But I can't seem to find anything to answer my question (it most probably is because I lack the knowledge in this field).
So here are the two main questions of this problem:

When created, can the mRNA vaccine have flaws and when injected generate a different spike protein than the SARS-COV2 one ?
If so can the spike protein be harmful to our system in any way ?

I am sorry for any term not correct in this context.

The mRNA won't be entirely perfect, but the imperfections will not matter.
The spike protein is big, encoded by thousands of base pairs in the virus. In the virus itself, it's not entirely homogeneous: there are always going to be small mutations that cause different variants to be produced, but nearly all of those are nearly identical.
The mRNA in a vaccine may also have some degree of copying errors introduced during amplification, which will produce some distribution of variants. Though the specifics are different, random copying errors in a synthetic process and random copying errors in natural viral replications will produce qualitatively similar types of distributions (more serious errors producing truncations and recombinations can occur in both as well, but similar arguments apply and they're even less likely to be functional).
Moreover, since only the spike protein is there, it can't actually produce a damaging infection, only teach your immune system what an infection looks like. Finally, since it's easy to validate a batch of mRNA via sequencing, ordinary quality control procedures should be fine to make sure what goes into the vial is what was planned (modulo the variances described above, when they are at a low enough frequency to fall below the threshold of discrimination).
In short: don't worry about the mRNA varying. If you're going to worry about something, worry about the virus varying enough that our nice, tightly controlled mRNA doesn't match it any more.

This answer providea no evidence in support of the statements made, so that although the poster may have accepted it, he has no basis on which to assess whether or not it is correct. Furthermore, by  repeating the unusual term "flaws", without any explanation of what is meant or how you imagine they arise, your answer lacks conviction.

@David What additional details are you looking for? I typically try to answer questions at a level appropriate to the apparent expertise of the asker, thus focusing on what I perceived to be the core of the question, rather than going into full details.

@David you are right I have no basis to really know whether or not this is a good answer. But Jake you can also go into full details, I will read and research terms I don't know of yet.

I would prefer a detail answer even if I can't get everything than an incomplete one.

I've added additional detail to explain the reasoning more thoroughly and precisely.


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Glycolysis step 5: isomerization by triose phosphate isomerase
On the 5th step in glycolysis, triose-phosphate isomerase converts dihydroxy-acetone-phosphate to glyceraldehyde-3-phosphate.
Now my question is: Why?
Most books and sites I've read only say that glyceraldehyde-3-phosphate has a direct pathway compared to dihydroxy-acetone-phosphate. Anyone with additional info on this would help much if they shared.

Can you please clarify your question? Actually I am not sure, if I understand what you are asking.

Welcome to SE Biology. Unfortunately your question is unclear and does not yet meet our standards. It could be made to do so if you edit it. First, as a new poster, you should take the Tour and read the Help on Asking Good Questions. You should also look at other questions on the site where you will see that we use standard English here, not textese. Most important, we cannot explain statements you encounter in your reading unless you quote word for word and name the source (with a link if possible).

Thank you .I'm new, I will read through the guidelines and try to rephrase the question.

"a direct pathway" to what? If you consult a text to complete that phrase you will most likely see the answer to your question yourself. In any case wiithout completing it your question is still unclear, regardless of any scatter-gun answers that are posted.

"Why" questions in biology tend not to make sense-
https://en.wikipedia.org/wiki/Teleology_in_biology
But perhaps if I narrate the reaction it will connect with your intuition.
Let's look at the reactions in question:

https://en.wikipedia.org/wiki/Glycolysis#Summary_of_reactions
Step 4 in glycolysis cleaves fructose 1,6-bisphosphate into two molecules that are isomers. One isomer (glyceraldehyde 3-phosphate, GADP) is a reactant in step 6, and fuels the “payout phase” where glycolysis reactions begin to yeild ATP and NADH. So what happens to dihydroxyacetone phosphate (DHAP), the other product from step 4? How can we extract energy from this?
Reaction 5 is the interconversion of GADP and DHAP. So as GADP is consumed by reaction 6, reaction 5 will, by Le Chatlier’s principle, lead to net conversion of DHAP to GADP. The GADP produced by this isomerization then also feeds reaction 6. In this way, both of the products of reaction 4, GADP and DHAP, are channeled down the chain to fuel NADH and ATP production.

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How do I homogenise a small pellet of 10 to 50 cells within less than 50 µL?
I have a problem with declumping/ homogenising bacterial cells in small volumes (10 to 50 µL). I know that I can get all of my cells out of the tube, but they are still stuck together and won't form separate colonies on an agar dish.
I know that because when I take the last 50 µl from a 1 ml tube and put it in a new tube and mix the 50 µL with a larger volume (e.g. 100 µL), we get a higher CFU count.

Just to be sure: is it really 10-50 cells in your pellet? Or is this a typo and its rather 10-50 x 10^6 cells  or similar?

Thanks for the quick answer! Yes, there are only 10 to 50 colony building units in the 50 µL pellet!

What homogenisation method(s) did you already try?

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Blosum matrix computation with X%
Why does the answers to the problem found in the referenced pdf, differ from my calculation below? I am trying to understand the math from this pdf from an online tutorial I am reading and my own math does not give the same result: Can someone help derive their answer or confirm mine?
http://www.cs.columbia.edu/4761/assignments/assignment1/reference1.pdf
On page 13, I am trying to figure out how the weighted values are determined:
For example C_LL: 2.33 means the construct is [L_1   (L_2a L_2b)  L] and the center block is being counted as 1/3 for each so we get 4*(1/3) + 1 = 2.33 but the L_2a to L_2b i.e., the inside the block is not counted that should make it 2.66 right?
For C_LV: here there is obviously 4*1/3+1 and now the internal would be 2*1/3 which sums to 3 not 3.33. And now the internal one is counted.
I am confused. Any help?

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Name for a set/collection of eggs which are laid and receive no nurturing of any sort by parents
OK - so, mammals have litters, and they look after their young.
Hens (birds generally) have clutches and many/most look after their young.
Octopuses have broods since the female looks after the eggs, but expires
just as they hatch!
The thing I want to know is:
What is a group of eggs laid by a creature which just lays them and
moves on called?
Also of interest would be such creatures which lay single eggs periodically (is there a difference?).
I'm particularly interested in insects and the like, but any additional
words which may apply would be of interest, and yes, I have Googled but
to no avail!

Hi and welcome to Bio.SE! This is a very broad question and likely has many thousands of correct answers. Perhaps you could help narrow things down by explaining why you want an answer to this question.

@James The reason I'm asking is because the info-graphic here makes reference to the "average litter size" of the octopus. I told my lecturer (a comp. sci. person) that mammals had litters. I could only remember the word "clutch" for eggs, but didn't think that applied. After thinking, I came up with "brood" for octopuses. However, it led to me wondering about what one calls a set/collection of eggs that are just left by the female without any further nurturing. Octopus mothers brood till hatching, then die, but there is input!

Mammals generally nurse their young at least to some degree. I can think of no examples where mammalian young are left to fend for themselves immediately after birth. The names of groups of the young of animals is incredibly inconsistent, so I doubt this answer would have any roots in biology! It would be interesting if someone could prove me wrong.

@James - I've edited the question title. Mammals don't apply. Some birds may. Many insects lay the egg(s) and play no further role in nurturing the eggs/offspring! I want to know what is the set of eggs laid called - IMHO, it's not a litter, *nor a clutch nor a brood!

Perhaps you'd have more luck over at the English language SE?

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What is this (water-loving) bug?
For some time we've been finding these little fellows in our apartment:

They seem harmless enough, but finding them is a bit... annoying. I found the fellow above in the bathtub, and it's not uncommon to find more than one.
Unfortunately, some started to appear near the kitchen sink as well. Or outside of the bathroom on the floor (at least that's where we noticed them).
I think this thing prefers darkness over light, and seems to be drawn towards wet places or just water. These critters are also surprisingly fast.
What is it? Should we be concerned about a pest problem, or is this just a minor, unwelcome guest?
PS. We live in Poland.

It is a Lepisma saccharina or silverfish.
It is rather common and yes, it's harmless.

This answer would get more upvotes if you added a picture and perhaps addressed why the OP is finding them in wet locations in their home. In other words, it'd be good to "beef up" your answer a bit :).

@theforestecologist While you'd generally be right, as the OP I find the Wikipedia link to be a very good answer. After reading through the Wiki article I found it not surprising at all - the bug likes wet places, darkness and is fast (all 3 characteristics that I listed). No surprises then that I find the things in the bathtub or near the sink...


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Albinism inheritance problem: what are the father's alleles if he got an albino kid?

Albinism is caused by a recessive gen "c". A normal man marries an
  albino woman. The first son happened to be albino. What are the
  possible phenotypes of the parents? What is the chance that their
  other kids will be albino?

Alright, since "c" is recessive and the woman is albino, then the woman must be "c c" right? And since the son is albino, he must be "c c" too. Hence the father must have at least one "c". But since he is normal, then the other allele must NOT be "c" too (otherwise he would be albino).
My question is, when writing the Mendel table, how do I express that allele of the father (the one that is not "c")?
$$\begin{bmatrix} & c & c\\
? & ?c & ?c\\
c & cc & cc\end{bmatrix}$$
I marked it with $?$ because I'm not sure what to put there. My first thought was "well, it could be a capital C I guess..." - but that doesn't sound right to me. A capital C would mean there is a dominant albinism allele (but I am told that albinism is recessive only...)
I can see clearly that there is a 50-50 chance of having albino kids. I just don't know how to draw that inheritance table.

Super oober short answer: The father is Cc, the mother is cc, there is a 50% chance the children will be albino (as you predicted).

An explination on Mendelian genetics:
First let's look at (what a lot of people consider) the normal Mendel table from here:

Since the dad is normal, that means he has at least one Normal Gene. Which makes him C ? . We also see that mom is normal, so that means she also carries the gene C ? . In this case, they wind up with one child that is affected which means the child has the trait cc. That means both parents had to give the child one little c so that makes both of the parents Cc.
Your answer:
Now, in your problem the mother is albino, which you correctly put as cc.
The dad is normal, which means his C ?. He could eaither be CC (homozygous dominant - an uneffected non-carrier of the affected gene) or he could be Cc (heterozygous - an uneffected carrier of the affected gene). So at this point all we know about the father is that he is C ? . Which means you were on the right path.
Now we look at their first son. We are told he is albino. That makes him cc. That means that the father HAS to have at least one affected gene making him Cc.
So you were correct in thinking that it was Cc. You tripped yourself up by saying that it would make albanism the dominant. As you were told Albanism is a recessive gene. The big C is the normal gene which would hide the albanism trait.
To draw your table, just change all of your ? to big C.


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Is there non-coding DNA common to all living things?
I saw the question asked about proteins common to all life, and was happy to see there are proteins common to all living things. Similarly, I wonder if there are portions of non-coding DNA that are common to all living things too.
PS  This was NOT a homework question as the feedback indicated.  I was curious to know and didn't know where to turn so I asked Stack Exchange.  I am not a student, just a person who wants to understand life better.

Relevant link https://en.m.wikipedia.org/wiki/Conserved_non-coding_sequence

There is an answered question about such conservation in eukaryotes here: https://biology.stackexchange.com/questions/2607/ . An intelligent reading of the answer suggests why this is unlikely to extend to prokaryotes.

@Jon unfortunately on SE.biology there is a confusing close vote reason which uses the term "homework" to really mean 'under researched'. I know that is confusing and irritating when your post gets closed using that reason when it is not a homework question. My advice would be to google around for an answer, show what you found and what you didn't understand, and then hopefully the question can be reopened. perhaps start with the wikipedia link I shared in the comments.

Thanks for explaining.  I did google around but just missed the answer I guess.  Anyway, no need to reopen since your comment pointed me to the answer.  Thank you!


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Protostomia classification and characteristics
While working through a practice test for my final exam in an introductory organism biology course, I came across this question:
Protostome characteristics include which of the following?
a) a mouth that develops secondarily, and far away from the blastopore
b) coelom formed by schizocoely
c) radial body symmetry
d) spiral cleavage
e) none of the above
After reading the answers a few times over, I just moved on because I couldn't figure out how to answer. My first instinct said that both (b) and (d) were correct, but the answer is (e).
After some thought, I've come to a few ideas how this could be true.
1. The wording is incorrect, the definition he provides for protostomia says "body cavity formed by schizocoely," and "spiral determinate cleavage."
2. These two characteristics are not present in all protostomes (i.e. spiralia evolves after ecdysozoa, and platyzoa have no body cavity).
Just looking for some clarity or closure regarding this.


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Does the edge effect promote biodiversity?
I define the edge effect as:
A term used to describe what occurs at habitat boundaries where two bordering communities influence one another.
My question is whether it generally leads to an increase or decrease in biodiversity (both evenness and richness) and why.
Also, what are the biogeographic factors that impact biodiversity relating to this edge effect?
I believe that species diversity would increase, as at such habitat boundaries species that inhabit the bordering habitats and those that can also be found in habitat boundaries would be present.
I do remember reading that light intensity increases due to the edge effect and thus also allows for shade-intolerant species to thrive, but I do not understand why.

The question is interesting. The question might be considered as too broad but to even start thinking about the question we'll need a definition of biodiversity. Biodiversity can mean many different things. Did you mean number of species per square meter or something like that? There might have issues with what you would call "different communities" too. Also, if you can include thoughts (if any) and what you've found so far (if any), it may help.

EDGE EFFECT PROMOTES BIODIVERSITY.
EDGE EFFECT OCCURS IN ECOTYPE.
ECOTYPE IS THE TRANSISSION ZONE WHERE TWO COMMUNITIES MERGE.
HENCE SPECIES RICHNESS IS FAIRLY HIGHER THAN THAT OF THE SURROUNDING ECOSYSTEMS.
IF ANY OF THE SPECIES TENDS TO EXPLOIT THE RESOURCES OF THE ECOTYPE IT WHOULD HAVE TO MODIFY ITS CHARACTERISTICS BY THE PROCESS OF  ADAPTIVE RADIATION AND EVOLUTION .
HENCE NEW SPECIES EMERGES PROMOTING BIODIVERSITY.

You have something that needs fixing.

Can you please edit your answer and fix the typing? All caps is hard to read.


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Why are considered to be exceptions to the cell theory?
If I am not mistaken, the cell theory states that:

All living organisms are made up of one or more cells
Cells are the smallest units of life
Cells arise from pre-existing cells

Aseptate fungal hyphae, giant algae and skeletal muscle fibres are often used as examples of cells that do not conform to the cell theory
(as explained in the first section on this site: http://www.patana.ac.th/Secondary/science/IBtopics/IBCell%20(01)/Pages/1.1.htm)
I am aware that the listed cells  are unlike the "standard cell" (e.g. large, many nuclei within one cell), but how do they go against the three points in the cell theory? (as there is no mention of how they should appear in the theory)

The theory is old and obsolete. When it was postulated many of these examples were not considered. This is the age of molecular cell biology and you very well know that all these tissue types do conform to the same basic cellular principles. I do not understand the point of your question.

Skeletal muscle is a tissue, not an organism. Your title is lacking a noun making it incomprehensible. You do not cite a source for the contention  that aseptate fungi and giant algae are not considered cells. Please clean up your question.

If you are looking for a hard and fast answer, there is none. Life does not have a hard and fast definition, so it is impossible to identify something that everyone will recognize as both living and non-cellular. However, your question is answerable if you are interested in a summary of the state of the debate.

All living organisms are made up of one or more cells

An exception to this would be known as non-cellular life. Whether anything could or does fill this category is a controversial subject. Considering the fact that the main points included in most definitions of life are based on observations of cellular life, this is not surprising.
That said, the strongest candidates for non-cellular live (in descending order) include: viruses, viroids, and prions.

Viruses are the non-cellular entities most often considered potentially alive. Viruses are even classified in genera and species. They carry genetic material, they evolve, and they use various proteins as their machinery of action. However, they are unable to metabolize or produce their own proteins. They depend on infected cells doing all the work for them. Because they are incapable of acting on their own, they are not considered living by many. (The definition for life usually includes metabolism, the ability to process one's own food and energy.) The counter argument is that all life ultimately depends on external factors for survival, so viruses depending on cells for living may not be a disqualifier since they still control the processes resulting in their reproduction.
Viroids, like viruses, depend on other cells to carry out metabolic and reproductive processes for them. Unlike viruses, viroids lack any protein whatsoever. As a result, even fewer people are willing to consider viroids alive. However, the same logic used to argue the biotic nature for viruses can be used for viroids. They copy themselves the same way many RNA viruses do, with the exception being they forgo directing the construction of any protein coat for themselves. Conversely, viroids can also be used as evidence against even viruses being considered life, precisely because of their similarity. If a viroid obviously is not life, viruses must be held suspect since they can be argued similar to viroids than cellular life.
Prions are interesting. They do not reproduce like viruses or cell. That is to say they do not direct cellular machinery to construct copies of themselves. Instead, they modify existing proteins they come in contact with. From one angle, they are far less active in their flavor of reproduction than viruses. However, they are also more directly involved in their self-replication than viruses. Also, they can spread between organisms. Mad cow disease is a well known example of this.

Back and forth arguments aside, it has become fairly common to view viruses as a sort of middle ground between life and non-living processes, not one or the other.

Cells are the smallest units of life

This one is not quite separate from numbers 1 and 3.

Any non-cellular lifeform could be used to ague that the cell is not the most basic unit of life.
Similarly, a cell not originating from a pre-existing cell could be used to make a similar argument, because it is highly unlikely that all the process found in even the most basic cell could start from scratch. They would have needed to exist before the cell in question, and then become incorporated into the cell. This rational is the basis for hypotheses like the RNA world, which are used to explain how life's processes could have been started, in piecemeal fashion, before being locked in cells.

Of course, we can also used the above points to argue that the cell is, indeed, the smallest unit of life.

Viruses, viroids, and prions can be used to support the assertion that cells are the smallest unit of life. Even though they are not cells, their reproduction is only made possible by the activities carried out within cells.
Things like the RNA world (if real) only would have required the processes for life gradually building up from less ordered, spontaneous reactions. An RNA world could be argued as a world devoid of true life, since life can be argued as things which carry out several key processes, and not as merely the individual processes themselves.

Cells arise from pre-existing cells

This one is the only easy one. This had to be violated by abiogenesis. There had to be a first cell (or group of cells created under common conditions).
The origins of the first cell(s) are variously explained by the RNA world, GADV-protein world, and other hypotheses. Whatever the case, however life started, it had to have a start. This means there must be one or more cells in the history of life that were spawned from some natural processes lacking a parent cell.
While it may be safe to say that all cells in history are not required to have had parent cells, it is also safe to say that it is extremely uncommon for parentless cells to come into being. Firstly, it is not something we have ever observed. Secondly, all indications point to all species being part of the same "tree of life." This would mean that whatever conditions spawned the first cells must not have persisted. Either all life descend from the same single cell, or life started with many independently spawned cells that blurred their independent origins due to heavy horizontal gene transfer.
We can view the cells from cells rule a bit like Newtonian gravity. It is mostly right, with its faults only becoming ovbvious under conditions not readily present on Earth.
EDIT:

Aseptate fungal hyphae, giant algae and skeletal muscle fibres are often used as examples of cells that do not conform to the cell theory
...
I am aware that the listed cells are unlike the "standard cell" ...

I forgot to answer this part, and I think it is important to do so. All of those conform to cell theory. Whether they conform to the pattern common to most cells or not is irrelevant. They all have the components required to classify them as cells. Cells merging into multi-nucleated cells (like skeletal muscle fibers) is actually a good argument for cells being the basic unit of life. Even though they start separate, they collaborate by becoming one cell. Sure, the resultant cell has multiple nuclei, but most cells on Earth have no nuclei.


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How do you know which organisms are keystone species?
I know that keystone species are those that play a crucial role in an ecosystem, but since all species are interdependent upon each other and each occupy their own niche, aren't they all important?
How do you know which organisms are keystone species?

According to the wikipedia page, a keystone species is:

A keystone species is a species that has a disproportionately large effect on its environment relative to its abundance.

Thus, you could work out the keystone species in an ecosystem by sampling population size and and what size 'effect' the removal of the species from the ecosystem would have. If you standardised the units of 'effect' for all species in the ecosytem, the keystone species would be those with the highest effect/population fraction. I don't know if there's a critical size of this fraction for a species to be determined 'keystone', but if there is it would allow you to explicitly define a keystone species. This would rule out the problem of interdependency as you mention.

(Posting different answer as it gives a different approach to the question)
Re-reading this I think you were asking about how we'd infer these keystone species experimentally.
As a starting point, one could apply network inference on species counts in the ecosystem (https://doi.org/10.1890/09-0731.1, https://doi.org/10.1038/s41598-017-07009-x, https://doi.org/10.1016/j.ecolind.2015.11.031, as examples). This kind of study returns networks which represent the interactions between species - you could then search through these networks for species with many connections in the network. Removal of a species with many interactions with many other species is likely to have a greater impact than removal of a species with fewer interactions, suggesting these are keystone species.
I realise in your question that you sort of imply each species has an interaction with every other species in the ecosystem, but studies like the ones above show that this might not be true. Or at least, many of these interactions may be indirect, via another species.
After such a study you could apply statistical methods like Pearson's Correlation to work out the 'strength' of the interactions in the network. From this could identify species with many high-strength interactions as keystones. Alternatively you could attempt a parameter fitting on the learned network structure (as you can in the case of Bayesian Networks above), to try and predict what happens to the abundances of other species if you remove one of your candidate 'keystones'.
Hope that gives a more experimental angle on how to solve this question!


text:
Based on this diagram, how do you deduce the keystone species?
How would you figure out what the keystone species is in the following textbook question? (questions 1 and 2 at the bottom of the image)
Based on my knowledge, a keystone species helps to maintain biodiversity therefore I think it is either the otter or the kelp that is the keystone species. I say this because when either one of them decreases in number, the other species decreases in number as well (less biodiversity).

What book is the picture/questions from?

From http://education.nationalgeographic.org/encyclopedia:

A keystone species is a plant or animal that plays a unique and
  crucial role in the way an ecosystem functions. Without keystone
  species, the ecosystem would be dramatically different or cease to
  exist altogether.
  [...]
  The sea otter is an example of a keystone species in the Pacific
  Northwest. These mammals feed on sea urchins, controlling their
  population. If the otters didn't eat the urchins, the urchins would
  eat up the habitat's kelp. Kelp, or giant seaweed, is a major source
  of food and shelter for the ecosystem. Some species of crabs, snails,
  and geese depend on kelp for food. Many types of fish use the huge
  kelp forests to hide from predators. Without sea otters to control the
  urchin population, the entire ecosystem would collapse. 1

The organism I would therefore hypothesize to be the keystone species is the sea otter.
The data supports the hypothesis as when there is an decrease in the number of sea otters there is a increase in the biomass of sea urchins, which is accompanied by a decrease in the density of kelp. The lack of otters feeding on sea urchins causes an increase in their abundance, and this leads to an increased consumption of kelp by the sea urchins, which leads to the decrease in the density of kelp. Therefore, the sea otter is the keystone species since a change in their abundance has a significant impact onto the ecosystem and the organisms living in it.


text:
What is the purpose of requiring two separate binding systems for the antibody response?
I've read that in most cases, B-cell activation requires helper T-cells.  This requires antigen binding by both antibodies and T-cell receptors, using two different antigen-binding proteins, recognizing two different epitopes.
Why is this so complex?  Would the overall antibody system still work if B-cells required only antibody/B-cell receptor binding?

Immunity can be a double edge sword. It is aimed to detect and destroy invading pathogens but it can also target the self, as exemplified in autoimmune diseases. To avoid this, many failsafe mechanisms exists.
For example, imagine an innocuous foreign antigen gets into your body and reaches the lymph node. There it may find a naive B cell that has a receptor that recognizes it. Without a double check mechanism this B cell will mature and begin to produce antibodies against this antigen, triggering an immune response that is not beneficial (e.g. in allergy) and is not necessary (the antigen is harmless).
Because of this, activation of the adaptive immune system requires usually two signals. In the context of B cells the other signal usually comes from effector CD4 T cells (of the type T follicular helper Tfh) and is called linked recognition, because both the naive B cell and the Tfh cell have to be specific for the same antigen.
So a possible scenario may look something like this: a pathogen's antigen is taken by DCs. If there is an ongoing inflammatory response this DCs will get fully activated (a process called licensing) and migrate to the lymph nodes. There they present the antigen to naive T cells. Naive T cells specific for the antigen mature and become effector T cells that may include CD8 and several classes of CD4 T cells, including CD4 Tfh cells. The antigen is also transported to the lymph nodes and presented to naive B cells. Naive B cells that recognize the antigen AND also are stimulated by Tfh specific for the same antigen then mature into plasma cells that secrete antibodies.
For harmless antigens, even though DCs may phagocyte them they will not get fully activated in the absence of an inflammatory response. So the activation chain is broken. This system fails somehow in the case of allergy.
Another point is that this mechanism is related to the generation of antibodies against microbial protein antigens. Animals lacking T cells cannot produce them and so they are called thymus-dependent (TD) antigens. Other microbial antigens like bacterial polysaccharides can induce antibody production without the help of T cells. This so called thymus-independent (TI) antigens provide the second signal by direct recognition of the antigen (e.g. through TLRs) or by inducing extensive crosslinking of B cell receptor (BCR). TI antigens include LPS and bacterial DNA. TI antigens appear earlier than TD antigens and although provide some protection they are less efficient than the TD ones because TI-specific B cells do not undergo affinity maturation and isotype class switching as TD antigens do.
Reference: Most of what I describe is found in Janeway's Immunobiology, 8th edition. Chapter 10 (The humoral immune response). In particular the section 10- "B-cell activation by helper T-cells".


text:
What causes the opaque green colour in Lepidoptera?
Link here to what I mean by 'opaque' colouration on the insect, the colour intensity remains constant despite changes in light intensity and angle (not shown by the picture but the moth exhibits this in the field). This is different to 'metallic' colouration on other moths like the Forester moth (image here), where the colour intensity changes with light angle and intensity.
Through reading R.F. Chapman's book ('The Insects:
Structure and Function'), I know that metallic colours are caused by interference patterns produced by the micro structure of the scales, the book says this is how most higher frequency colours are produced, including green in this category. Obviously I've looked for pigments that could give this colour but I haven't found anything that is produced in insects.
So my question is: Is there a pigment that gives this colour in the insect and if so, what is it?

According to this paper, green pigments are found in lepidoptera. The study focused on Geometridae, and found that the primary pigment in emerald moths, such as Hemistola chrysoprasaria is also found as secondary pigment in Pseudoips prasinana. The authors dubbed the substance 'Geoverdin' and suggest it may be a derivative of chlorophyll consumed during the larval stage. I cannot find any further studies mentioning 'geoverdin' or its chemical identity.


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How does cytochrome c oxidase inhibition cause cell death?
I realise the inhibition of cytochrome c oxidase prevents the release of H+ ions into the intermembrane space, and that the ion gradient is required for ATP synthase action. However, I'm not sure how this causes cell death.
Does this:
a) Prevent oxidation of Cytochrome C, preventing electron movement the cytochrome bc1 complex, which in turn prevents electron movement from earlier parts in the chain, shutting down the electron transport chain altogether? Thus, no ATP is produced and the cell dies due to lack of ATP.
b) Prevent oxidation of Cytochrome C, but not preventing oxidation in the other protein complexes*, merely reduce the number of H+ ions available for ATP synthase action, lowering the amount of ATP produced, and the cell dies due to low ATP levels.
c) other.
I realise in either case, the ATP count is merely lowered, as ATP is produced by other methods, so my statement 'lack of ATP' is not totally explicit.
*This being the case, how are the released electrons dealt with by the cell? Are there electron acceptors to remove this?

The cell dies due to lack of ATP but the organismal death happens because the brain and the respiratory centre is affected. Neurons are quite sensitive to ATP loss.

Thank you. Do you know exactly how inhibition reduces the amount of ATP? Is it scenario a), b) or other?

Inhibition is rarely binary - it's almost always subjected to stoichiometric effects. So the answer could be either option, depending on the amount of the inhibitor present in the system. If there is a huge amount of the inhibitor in the cell, it may more or less completely ablate ATP production by the ETC.
On the other hand, if there isn't enough of the inhibitor to shut down all cytochrome C oxidase, you'd only see a reduction in the amount of ATP produced by the ETC (which could still be sufficient to kill the cell).
It also depends on the type of inhibition taking place. Is it reversible or does it bind permanently? Does it degrade quickly? These aspects are also important to consider.


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Why does Citric Acid occur in Citrus fruits?
Why is there so much citric acid in citrus fruits? And how did it evolve i.e. what did it come from? Is it a by-product of the ripening process?  Why have citrus fruit evolved a particularly high amount of citric acid compared to other fruits? Was it due to particular selection pressure for acidic fruits or was there a genetic bottle neck that caused this such as human cultivation?
I've been trying to search for this but google scholar isn't throwing up anything so I'd really appreciate some help.

This is a related question but I don't think the answer there has addressed the evolutionary aspect of acid accumulation.

Thank you for the link anyway, the answer may give me some useful information.

It's been a difficult search, honestly. I'd like to think the citric acid preserves the fruit in it's native growing condition; lemon trees originate in Asia, for example (high humidity, lots of bugs, etc.). I've come up largely empty-handed!

Actually citric acid is not only available in citrus fruit but also in pretty much any living thing. it is an important intermediate in Krebs cycle, but I guess the main reason that it is available in high concentrations in citrus fruits is because citrate is an inhibitory compound for phosphofructokinase, that means it stops the glycolysis and hence it makes it hard for bacteria to use the fructose available in the fruit body.
Source:
 Stryer, Lubert; Berg, Jeremy; Tymoczko, John (2003). "Section 16.2: The Glycolytic Pathway Is Tightly Controlled". Biochemistry (5. ed., international ed., 3. printing ed.). New York: Freeman. ISBN 978-0716746843.

Then why haven't more fruits evolved this? I'm aware that citric acid is found in all living things, I apologise if the wording is misleading. My question more why does citric acid occur in such high concentrations in citrus fruits compared to other fruits.

Actually, I think  it is more a question of diversity. most of the fruits have their own preservatives, in citrus fruits case it's citric acid.in some fruits it's high sugar concentration.in some other it's vitamin C. it's a matter of diversity and the reason that other fruits went down another path is probably a matter of chance and environment and previous terms.
I hope I had answered conveniently.

@Phototroph I think by asking "Then why haven't more fruits evolved this?" you are making your question opinion-based. You might want to read http://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont for help. In short, evolution is not meant to make organisms better, but just to become different from others. Its natural selection by which better ones survive while worse ones can't.

I realise how evolution works, apologies if my wording doesn't make it clear. Haven't contributed further to this because Shayan's comment more or less answers my question (it's a question of diversity), but have left this open to see if anyone else has anything further to contribute


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Soft Agar Substitute
I've got petri dishes with a base agar layer ready for E. coli culturing. However, I do not have soft agar in which to dilute the E. coli before pouring it on to the plate.
Any suggestions on what substance I can use to substitute for soft agar, or how I might be able to make it? I have the following at my disposal from the lab at school:

Tryptone base agar
Nutrient broth
MacConkey agar

The original soft agar medium had the following composition:

10 g Bacto™ tryptone
9 g Bacto™ agar
5 g KCl
1000 mL water

You want to take up the cells in a medium containing agar and then plate them?

@Chris Yes! I was originally using a soft agar solution composed of 10 g Bacto™ tryptone, 9 g Bacto™ agar, 5 g KCl, 1000 mL water.

And I guess that your standard plates are made with your media + agar?

@Chris Correct, the E. coli in the medium is poured over the base agar so the standard plates have the media and the agar.

Ah, I prepare the plates with medium + agar.

The good news is: You don't need any agar in your plating media, since the bacteria grow on the surface anyway and the plate can take up some additional moisture from your plating media.
What I usually do is to dry the plates for a while (and also let them warm up, since they are stored in the fridge) with the plate upside down and opened a bit. Contamination is usually not a problem here.
Then I dilute the cells in an appropriate volume of media, then plate about 50 to 100µl on the agar and spread it with a Drygalski spatula. Put the plate in the incubator and everything is fine.


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Why doesn't hair grow all over your face?
Why doesn't hair grow all over your face?
Surely hair on a face would have blocked the sun and kept it warm.
Or perhaps through natural selection we opted for hairless faces over hairy ones?

Why doesn't hair grow on the face- because there are no hair follicles in that region of the skin. Actually, in males the hair does grow all over the face except the eye region and forehead. Hair in those regions would block the vision.

Actually, we do have hair over most of our faces - it's just mostly vellus hair and not as visible.


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Why do we produce so many sperm?
So apparently we produce roughly 300 million sperm daily. Is there a reason why this is necessary? Wouldn't a much smaller (but still large) number be sufficient? Like, one million?

Can you add a source for this number?

@Chris it's something they just taught us in the biology class (I imagine it is also in the book http://www.amazon.com/Biological-Science-MasteringBiology-3rd-Edition/dp/0321543270). Google searches yield ranges from 80 to 250 million - either of these numbers serve the purpose of my question though. I don't really care how many are produced, but rather, what's the point of making so many.

The one winner out of millions is more special than the one out of two :)

so the question is, how does 300 million sperm cells are better than one? like, one sperm -- one egg?

@aaaaaa yeah exactly :D

It's interesting that you think 300 million is "so many" but 1 million is not. My point is, one's intuition for what is a "reasonable" number of things in nature is often a poor guide.

@Chelonian "Wouldn't a much smaller (but still large) number be sufficient? Like, one million?" I don't think I ever said one million is a small number. I said it is much smaller compared to 300 million. So the question is mostly about whether or not a much smaller amount would be sufficient.

One might guess that it is simply a hangover from fish doing external fertilization.  Evolution is not intelligent design: if something works, it tends to be conserved even if it is not 'perfect'.  To get to say 1 'sperm' fertilizing 1 egg, you'd have to back down a bunch of evolutionary paths, and take different branches...

@Voldemort Notice I didn't write that you said 1 million is a small number. I said that you didn't think it was "so many". Which was the case, wasn't it?

@Chelonian no, I never said that 1 million was not "so many". I said that it is much less than 300 million, but still large. So yes, I think that 1 million is still "so many", and the question is therefore "why not 1 million instead of 300 million? Both numbers are still massive"

@Voldemort Fair enough. My point about our intuition not being a good guide to what the numbers for things like this ought to be still seems applicable to human intuition generally; that is, why should 1 million, for example, be enough? Why not 24,500? The point is, the numbers are what they are, and maybe 300 million is the appropriate number (or maybe the system isn't optimized?).

https://biology.stackexchange.com/questions/39612/why-are-so-many-spermatozoa-produced-when-only-one-of-them-fertilises-the-ovum/39618#39618

The term you should look up is sperm competition, there is an introductory wikipedia article about it here, where you can get the basic picture and get some references to explore.
Simply said, males often compete with other males in the reproductive tract of the female, thus a higher number of sperm will lead to a higher chance of fertilizing the female in competition with other males - leading to an arms-race of the number of sperms a male eject into the female.
There is a lot more to it, of course, but I believe this well explains the most fundamental driver of why males generally produce and eject so many sperms.

If a male mates with the female, and then comes another male, wouldn't the first male be much more likely to succeed because he introduced the sperm beforehand? I imagine that just a few hours are a huge advantage, so I'm not sure why would one need so many millions of sperm anyway.

@Voldemort I think it's safe to say that any advantage of being first for a certain amount of time would be highly dependent on the nature of the species in question. But if the production of sperm is relatively cheap and the competition is relatively significant, I think it's easy to see that we might reach an arms-race here, even if the amount of sperm would not always have to be the most important factor.

@Voldemort And if we look at humans as an example, we are curiously unique in an unexpected way as our penises seem to have evolved to displace semen of other males from the vagina, so sperm competition seems to be very real even in humans.

Great reference Alex, right on track. Also high production of sperm also has to do with male health and dominance. In the wild a more dominant healthy male will produce more sperm and healthier sperm. Females pick up on this and will want to mate with someone strong. I'm humans this characteristic is not as widely perceived but women will tend to be attracted to a male that seams strong because psychologically he can " protect her and their young" of course we have evolved to money being a statement of power and dominance thus this can also serve as competition. All in all it boils down to ove

The answer, if you search for a bit, boils down to geometry. It takes X amount of sperm cells to successfully fertilize an egg. If you optimize delivery system (e.g. vagina geometry), you'll need less. In species where one male fertilize number of eggs (aka polygamy) and are able to have progeny from number of females, you need less cells in ejaculate to produce single child, because chances are higher with higher number of matings.
In humans it is quite often one male-one female relationship, so you have to bump number of cells in ejaculate so that mating season is fruitful.
Final point of real-life statistics:

Of the 300 million sperm ejaculated, only about 200 or so will survive to reach the egg cell and only one will succeed in fertilizing it.

You need to beat these odds ($10^{-6}$) in order to reproduce. Why female reproductive organs are so restrictive? Probably because there is some link between male's overall fitness and number of sperm cells. Fit males (those that hunt better than others) are able to spend more energy for generating sperm, rather than "feeding" their own body. If they able to "feed" 300 million sperm cells, they probably will be able to feed a child.

Your theory seems to go straight against the sperm competition theory?

I'm a bit suspicious of the implied statistics here... If there were 300 million sperm, and 40 million reached the egg, still only 1 would fertilise it (except in rare cases). Also you're relying on something like bodily system integrity to imply sperm count reflects general fitness. I'm not sure if something like this has been demonstrated. I'd be very interested if you could provide a citation for that line.


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How can plants be grown in hydroponics, and yet not handle too much water in soil?
It's pretty much common knowledge that plants planted in pots or soil that doesn't have good drainage can't be watered too much, or they'll "drown". Regardless of what actually happens, experience seems to show that it's true that plants planted in soil can't handle too much water in the soil.
Yet on the other hand, in hydroponics, plants can grow and grow very well indeed with their roots entirely submerged in water. Clearly, it's not about "drowning".
So what's the deal? Why do soil-planted plants die when they're watered too heavily?
(I wasn't sure if this is a Biology.SE or Gardening.SE question, but I figured it was biology since I'm looking for a more theoretical answer about what happens to the roots, rather than practical advice.)

I would actually recommend deleting this post and asking on Gardening. I'm sure users there have a much greater understanding of the mechanics of hydroponics than biologists might.

In hydroponic methods which submerge the roots, the liquid medium is oxygenated with an air pump (as in an aquarium) to provide the roots with oxygen, without which they stop functioning.


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What leads to the different types of navels?
Obviously, there are "innies" and "outies" in the human belly button world.  Both are the result of a knot tied in the umbilical cord just after birth.
But why do some belly buttons become outies while others become innies?  Is it related to how the doctor ties the knot, or is it related to how the knot heals?

In my opinion, this question doesn't belong here.  Biologists, and biology itself, are not responsible for belly buttons.  Doctors are.  Thus, the question belongs where I asked it - on the Health.SE.  However, I will be indebted to anyone who can answer the question, wherever it happens to be.

After childbirth, the umbilical cord is either tied (similar to a tourniquet - the cord itself is not tied into a knot) or clamped to cut off the blood supply. It is then cut distal to the clamp/tie, separating the child from the rest of the cord and the attached placenta. The remaining cells die and dessicate, and the stump eventually falls off, forming the umbilicus or belly button. The default result, barring any issues, is an "innie". However, an "outie" may form if the child was born with a tiny umbilical hernia, or there was a small unnoticed infection at the base of the umbilical cord. Either of these could lead to the formation granulation tissue, described colloquially as an "outie". People can also have combination navels, with the indentation of an "innie" but a small amount of protruding granulation tissue inside.


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dAT joining: please define
I came across a reference to dAT joining in my reading of Genentech by Sally Hughes. The technique is described in passing as a technique for joining DNA fragments used around the late sixties to early seventies (likely prior and after, too, of course).
A quick query into earlier visits of the topic on the exchange returned no relevant results, but the results may have been have been obscured by the copious references to the neurologic "DAT" term (dopamine transporter).
Please provide a quick explanation to this concept/technique if you're familiar.

In the context of this book, dAT joining is a method used in molecular cloning to join two DNA molecules. Basically, terminal transferase is used to add polyA or polyT to the 3' ends of each DNA molecule. This creates cohesive ends which can anneal and then be ligated together, giving a covalently closed circular DNA molecule.

Image from: Jackson DA, Symons RH, Berg P. 1972. Biochemical Method for Inserting New Genetic Information into DNA of Simian Virus 40: Circular SV40 DNA Molecules Containing Lambda Phage Genes and the Galactose Operon of Escherichia coli. Proc Nat Acad Sci USA 69(10):2904-2909.
See also: Lobban PE, Kaiser AD. 1973. Enzymatic end-to-end joining of DNA molecules. J Mol Bio 78(3):453-460.

dAT joining can also refer to an assay of DNA ligase activity. Linear dAT oligomers are incubated with the ligase, which can circularize them and make them resistant to exonuclease digestion. This resistance to digestion correlates with DNA ligase activity.
Modrich P, Lehman IR. 1970. Enzymatic Joining of Polynucleotides. J Biol Chem 245(14):3626-3631.


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Open database of medical images
Does anyone know of an open repository of medical images (e.g., CT scans) organized by disease category? I'm working on some computer vision software that requires a large set of controls from which to learn.

Try this -- http://www.nlm.nih.gov/NIHbmic/nih_data_sharing_repositories.html

Similar: What are good sources of free-to-use images and diagrams

Searchable database of Point of Care Ultrasound (POCUS) Images: https://www.grepmed.com/?q=POCUS

https://opendata.stackexchange.com/questions/6661/open-source-mri-image-dataset/13565#13565

Open-access medical images:

MedPix (by keyword, organic system, pathology and diagnosis A-Z)
Radiopaedia (by keyword)
PEIR Radiology (by keyword, organ or anatomic region)
Ultrasound Cases (by keyword and organic system)
Open Access Biomedical Image Search Engine (Openi) (by keyword)
Wikimedia Commons (by keyword)
Google image search (using the filter "creative commons," "public domain" or "open access")
Google image search (using filters: black/white, noncommercial, photo)

More:

Gray's Anatomy
Dermatology Atlas

+1 Nice collection. I won't add google image search in the list though.

I have used that search extensively with good results, because you can find pretty much all free images available on Internet in one go. And it's easy to narrow the search down.

Here's a good start: http://www.aylward.org/notes/open-access-medical-image-repositories. I understand that this question was somewhat googleable, but perhaps amassing a collection of curated resource links is constructive here since a search through the exchange revealed no prior inquiries into this topic.
Update:
For those who are interested in understanding the current landscape of tools available for analysis of medical images: Check out this list of open source tools (http://www0.cs.ucl.ac.uk/opensource_mia_ws_2012/links.html).

Like I already referenced on an early post, there are several options on the DICOM Library. It is easy to find whatever image modality you want and also whatever disease category.


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What is the difference between the evolution of fins in whales and fish?
For a homework assignment I received the following question:
Which statement best explains the evolution of fins in whales and fish?
a. The common ancestor of whales and fish possessed genes for fins.
b. Whales and fish possess the same mutations in their genomes.
c. Fins evolved in whales and fish because they both use them to swim in water.
d. Fins evolved in whales and fish because of different mutations that occurred
in their genomes.
e. Fins evolved in whales and fish because their most recent common ancestor swam in water.
My answer is (c). Of the given options, it seems most accurate. I feel that the language is unclear as many organisms who do not have fins swim in water. That can be a logic against the option. But, the given answer is (d). That seems too bizarre as even humans and fishes have different mutations in their genomes. (c) seems more appropriate as it can exemplify convergent evolution.

FWIW, I agree that C is a better answer, because it demonstrates that you understand the concept of convergent evolution, and "different organisms have different mutations" is a pretty trivial observation.  It could be the answer to virtually any question you could ask about different organisms evolving differently.

It sounds like "d" isn't saying that having different mutations caused fins to evolve, but it's making a contrast to "b" - both whales and fish fins evolved via mutations that occurred in their genomes, but they weren't the same mutations in both lineages. Which is accurate. Is there a single answer or is this a "select all that apply" situation ?

I'm curious, have you asked your instructor about this question? Did they explain the reasoning for the correct answer and their reasoning why another answer is incorrect?

Short answer
d) is definitely correct.
Background
The crucial element is that whales returned from land to the sea and re-evolved fins.

a) is incorrect, as the common ancestor may not have had fins. In fact, it is thought it was a sea squirt, a sedentary species without fins, that was the most recent ancestor of fish.
b) is incorrect, as they may share some mutations but overall they have very different mutations and very different genomes altogether, being fish and mammals;
c) is incorrect as they have to develop fins first before they can use them;
d) is correct, as the emphasis in the answer is on

Fins evolved in whales and fish because of different mutations that
  occurred in their genomes.

Fins in whales have developed from arms and feet. Hence there are different mutations going on, as fish don't have arms and feet.

e) The common ancestor from fish and whales may have been in the water, but may not have had fins.

I disagree that "c" is incorrect. First, by the logic of "they have to develop fins before they can use them" nothing would ever evolve. Both whales and fish started out swimming with things that weren't fins (arms/legs for whales, some kind of appendage for fish), so selection pressure developed for swimming ability and those whose limbs were better for swimming did better, presumably swam more, leading eventually to the evolution of fins. "c" might be meant to be incorrect because it sounds Lamarckian as written, but the fact is, whales and fish swimming is integral to why they have fins.

Also for e): I'd say whether the common ancestor of fish and whales had fins is irrelevant - "e" is wrong because that common ancestor being in water isn't the cause of whales having fins. After all, it's our common ancestor too and we don't have fins. Whales have fins because their mammalian ancestors became aquatic, not because the first vertebrates lived in water.

actually all tetrapods have the genes for fins, limbs form as fins first then apoptosis kills the cells between the individual digits turning a flipper/fin thing into a hand or foot with individual toes. That's why thalidomide did what it did it intercepts the pathways for apoptosis.

@Rozenn Keribin: Also ichthyosaurs.  And FTM penguins started out swimming with wings.  So our original fish ancestor develops fins, which evolve into legs as Tiktaallik and friends move onto the land.  Ichthyosaurs and cetaceans go back to the sea and the legs re-evolve into flukes.  (Note intermediate cases like seals & otters.)  And penguin ancestors evolve their front legs into wings, and then into flippers...

Your answer is almost correct.. I do not like how you say "whales returned from land to the sea and re-evolved fins." Or how you said "Fins in whales have developed from arms and feet.".. These statements are basically the equivalent of saying that humans transformed from chimps. That is not how evolution works..

@Bob I'm trying to get a message across and I adapt the answer to the level of the question. Thanks for the lesson, but I'll leave at at this :-)

I agree with you that the question is ambiguous, and also that the most sensible answer would be C.  However, one could make a more or less reasonable argument in favor of several other answers, too.

a. The common ancestor of whales and fish possessed genes for fins.

Technically, this statement is true.  At least some of the fins of whales and fish are even distantly homologous, even though the lineages leading to tetrapods (including whales) and to ray-finned fishes diverged quite early in their evolutionary history.
(Specifically, the flippers of whales are modified tetrapod forelimbs, which are homologous to the pectoral fins of ray-finned fishes.  Whether one should also consider the tails fins of whales and fish to be homologous is a bit more debatable: the actual fin structures are very different, and presumably share few if any developmental pathways, but the tail and the spinal column which they attach to and are powered by is clearly a shared feature of both groups.)
However, while shared evolutionary history may explain why fish and whales have similarly placed flippers / pectoral fins, and why they both have a flexible spine that supports undulatory swimming with the help of a tail fin, it does not explain the convergent evolution of whales' forelimbs (which were formerly adapted for walking on land) into fin-like flippers.  So in that sense, while perhaps partially correct, this answer is also quite incomplete.

b. Whales and fish possess the same mutations in their genomes.

It's hard to even tell what this statement means.  Insofar as it's a restatement of the fact that whales and fish share some of their evolutionary history (up to the divergence of the bone-finned and ray-finned fishes), it's no more or less correct than statement A above.
However, I suspect that the intended meaning of this statement is that whales and (ray-finned) fish would've separately evolved the same "fin-making" mutations after their lineages diverges, which is both clearly incorrect and also, even prima facie, statistically very unlikely.  So I would rule this one out.

c. Fins evolved in whales and fish because they both use them to swim in water.

This statement is written using teleological language, which some may consider misleading, as it could be misinterpreted as implying that evolution was a directed process: it could be interpreted as saying that whales needed to be able to swim, so they chose to evolve fins (or that some guiding consciousness granted them fins).  This is, of course, incorrect — or, at least, we have no scientific evidence of there being any such conscious force guiding evolution, or of any organism (with the arguable exception of humans) being able to deliberately direct their own evolution.
However, it's quite possible to interpret this statement in a way that makes it perfectly correct: as both whales and fish move around by swimming, possessing fins (or something similar to fins) is an advantageous trait for them, and has thus been favored by natural selection.  If pressed, I would thus choose this one as the most correct answer out of the given options.
In particular, note that the argument made by AliceD that "they have to develop fins first before they can use them" is not really true: the ancestors of both whales and fish were swimming long before they evolved fins, and thus the selection pressure in favor of having fins (or fin-like structures) was already present before the fins themselves evolved.
In particular, the first aquatic ancestors of whales are believed to have swum much like modern-day otters and seals, using their flipper-like limbs as makeshift fins.  While there's no discrete transition point where one could definitely say that whale limbs turned into proper fins, it is clear that the fins, and their direct evolutionary predecessors, were being actively used for swimming, and that this fact directly drove their evolution into the actual fins that modern whales have.

d. Fins evolved in whales and fish because of different mutations that occurred in their genomes.

While technically correct, this statement is so vague that it's all but meaningless.  All evolution is driven by mutations, and those mutations, being basically random, are rarely if ever the same in any two lineages.
Certainly, it would be silly to claim that "different mutations occurring in their genomes" is an explanation of why whales and fish evolved fins: humans also constantly have different mutations occurring in our genomes, but we clearly don't seem to be evolving fins.  Neither are pigs or bumblebees or sunflowers, even though all of those species (and, of course, all others too) are also constantly experiencing different mutations in their genomes.
Really, this answer reminds me of the story about a person in a car who gets lost and stops to ask a passerby where they are; the passerby, after a moment's thought, replies "you're in your car."  While technically correct, that answer is absolutely useless — and so is this one, too.

e. Fins evolved in whales and fish because their most recent common ancestor swam in water.

Again, this answer could be interpreted as basically a restatement of answer A, and thus as being partially correct.  However, it completely ignores the convergent selection pressure described in answer C, which is responsible for the more recent evolution of whale flippers into something resembling fish fins more than, say, human hands or the feet of hippopotamuses (currently believed to be the closest living relatives of whales and other cetaceans).  Thus, I would not pick this answer, for the same reason that I wouldn't pick answer A.

Nice one +1. Great answer

While technically correct, [d] is so vague that it's all but meaningless. All evolution is driven by mutations, and those mutations, being basically random, are rarely if ever the same in any two lineages. Depending on the education level that the course was pitched at, the mere recognition that whales and fish have different lineages, and have not inherited fins (in their present form) from their common ancestor but rather evolved them separately, might actually be non-trivial hence credit-worthy. Many High School students would even go so far wrong as to think that whales are fish!

[Having said that, my first instinct on reading the question was the same as yours. The theme of the question suggested the examiner wanted to know if students understood the idea of convergent evolution, and (c) at least seemed to describe this, albeit in a verbally slightly clumsy way. I just felt that (d) is not entirely without substance, depending on the background the students are coming from!]

This was a question on the 2016 Toronto Biology Exam, precisely question 42.
Though the question was asked vaguely, d is the best answer. It's quite obvious that if animals are in water, fins will eventually evolve to improve fitness, that's pretty obvious.
However, if they are both in water, why are their fins different? This touches on the more complex concept of analogous structures; structures that perform similar functions but are anatomically different.
Well, why are they anatomically different? Different mutations in their genomes resulted in those differences.
Therefore, d is the better answer. It does ask which "best" explains.

It is far from inevitable that all aquatic animals evolve fins: marine invertebrates (jellyfish, crustaceans, octopus, starfish etc), sea otters etc (and possibly sea snakes, depending on your definition of 'fin').


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Is there an acceptable term for 'male fox' other than 'dog'?
I'm writing a lab on sexual dimorphism in Arctic foxes. As such, I use the words 'dog' and 'vixen' fairly often. In the discussion section, I compare the results from the lab with the results from research on other animals. The most relevant research I consider pertains to dimorphism among dogs (Canis lupus: the kind we keep as pets and their immediate relatives).
The term 'dog' denotes a subspecies of Canis lupus, males of that subspecies, and male foxes.
There are ways to disambiguate what I'm writing, but none of them are elegant.
I'm considering using 'tod' or 'reynard' instead. Are either preferred in biological writing? If not, is there an alternative?

could just say males and females... this is how I write when referring to flies in my writing. e.g. "...body size for males and females was measured
from..."

Female foxes are called vixen. But there is no specific term for a male fox. In fact, it would be much better to say "male" or "female" fox in a scientific context in which "fox" would mean the species, as rg255 suggested.

@rg255 WYSIWYG I was doing that initially. The problem was that males and females is ambiguous when comparing two or more sets of sexes (e.g. Arctic fox males and Arctic fox females with dog males and dog females). Specifying the species disambiguates things at the cost of brevity and doesn't solve the problem of repetitiveness (i.e. after some number of occurrences of 'males' by itself and in 'females', its repetitiveness becomes obnoxious.). I might just have to make do, but it would be better if there were an acceptable substitute.

Another thing you could try is using abbreviations like mF, fD, etc. These need to be defined of course...

It seems that we agree that there are no other terms within the realm ob biology. Would Academia.SE or English.SE be a better for this question then?

Just use "C. lupus" instead of "dog" when referring to that species.


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Would urination continue after death?
If someone was urinating, and they were to hypothetically suddenly "fall dead" (the brain is unconscious and all muscles / organs are unfunctional), would they continue urinating or would it stop?

Death of who? The person? The brain? Or the kidney?

@Superbest well the person of course. In 99.99% of cases I've read, "suddenly fall dead", refers to a person. It seems odd saying "if the kidney were to suddenly fall dead"

Many organs remain intact (and "alive" in that they can be transplanted) for minutes after brain death.

Yes. Moreover, even if they were not urinating at the time of death, they likely would at death, assuming adequate filling of the urinary bladder. There are two sphincters that close off the urethra. One is under control of the autonomic nervous system and the other is voluntarily controlled (somatic). At death, both sphincters will relax, releasing the bladders contents.

Related TVTropes. TVTropes warning.


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Why do carnivores evolve?
If humans can live without consuming other animals, then why do we do it? From a biological point of view, why do we eat meat? I would also extend the question to other animals because many animals are carnivorous: why did carnivory evolve and why do animals eat meat?

Answers to this question MUST cite a reference which should be either a peer-reviewed scientific article or a book. Unreferenced answers would be removed within 6h without notification. This rule is mandated because this is question, though quite interesting (and on-topic), is a popular topic that would attract a lot of opinion-based answers.

Because animal flesh provides a dense source of nutrients.  Evolution is amoral: anything that can be eaten, probably will be eaten by something.  Consider Darwin and the Ichneumonidae: https://en.wikipedia.org/wiki/Ichneumonidae#Darwin_and_the_Ichneumonidae  PS: And if you need a reference, start with "The Origin of Species" :-)

Besides that: Human cannot permanently develop and survive on a strictly vegan diet, since there are some important Vitamins which cannot be supplemented from vegetarian origin. Vitamin B12 would be a very important example, see this source.

@Chris That is incorrect, vitamin B12 is produced by bacteria, and in fact cannot be produced by any animal. You can get vitamin B12 supplements from a strictly vegetarian origin (https://en.wikipedia.org/wiki/Cyanocobalamin#Production).

@CactusWoman If you see biotechnical production as strictly vegetarian, ok. Still, vegetables (and fruit) still contain negligible amounts of B12 or B12 precursors and are not enough to maintain our needs.

@Chris I don't see why biotechnical production would not be considered vegetarian; the only requirement for a product to be vegetarian is that it does not contain meat. The vegan diet does need to supplement B12, but the supplementations are vegan, so it's incorrect to say "there are important vitamins which cannot be supplemented from vegetarian origin".

@CactusWoman: Are bacteria plants?  They don't meet the dictionary definition of plants, and many are capable of independent movement, like animals.

@jamesqf Vegetarianism and veganism is concerned with not consuming ANIMAL products. Bacteria are not animals. Fungi, plants, and bacteria are all considered vegetarian/vegan.

@WYSIWYG What is there to cite about "sometimes you live in a place where you can't find many plants to eat"?

@Superbest that is a layman's answer. You, as a biologist, can definitely say more than that.

Ana, evolution creates diversity (remember the diversification of Galapagos' finches). So, every available niche tends to be occupied, which includes carnivory.

A better question would be why wouldn't we eat meat, almost any animal will if given the opportunity, all but the most specialized herbivore can digest meat. Humans are good at acquiring food so why would we not eat something that is high nutrient density and easy to digest.

I'm going to focus on the why do carnivores exist part of this question, which should be extendible to answer why humans eat meat.
Let's start a thought experiment in which we only allow the consumption of vegetation (plants). In the simple system, we have our plants (lettuce) and our herbivores (rabbits). The lettuces have a constant population size and can support a limited population of rabbits. The rabbits satisfy their energetic and nutritional requirements by eating lettuces.
We then introduce a new species (humans) which are capable of eating both lettuce and rabbits (omnivores). If the humans limited themselves to only the lettuces as a food source they would have to compete with the rabbits in order to survive. Alternatively, the humans could hunt rabbits, as rabbits are also a potential source of energy and nutrition. The point being that, if a strategy has the potential to satisfy the energetic and nutritional requirements of a species, then that strategy has the potential to evolve. Because both plants and animals carry energetic and nutritional value, herbivory and carnivory/omnivory can evolve.

"All behaviour takes time. All behaviour consumes energy." [1]

Now consider the nutritional and energetic value of two the two food sources, plants and meat. Meat is typically richer in calories than vegetation, particularly those coming from fat and protein. 100 grams of lettuce contains around 14 calories, while 100 grams of beef contains about 200 calories. Protein is used by the body for growth, to repair tissues, produce hormones and enzymes and much more. Fat has a high energy content per gram (roughly twice as many calories per gram than protein or carbohydrate), is essential for the digestion of some vitamins,  and is an effective insulator. Given that behaviour takes time and energy, it is perhaps not hard to see that consuming meat can help to satisfy the energy requirements more quickly than consuming plants, allowing meat eaters more time for other essential activity like sleep and reproduction. Consider the activity of two large mammals, elephants and lions. Elephants spend a lot of time eating, some 12-18 hours per day (fortunately for them are quite able to eat on the move). Lions on the other hand typically hunt for short periods of the day (dawn and dusk), allowing them to avoid the heat (reducing water requirements), to rest, and reproduce.
Consider also that vegetation is often hard to digest — it is often is rich in cellulose. Many herbivorous species have complex adaptations to help digestion. Therefore, it's not necessarily easy, or easier, to evolve to eat only vegetation. Improved energy acquisition can evolve by both eating more energy rich foods and by more efficiently extracting energy.
Carnivory is also present in plants. According to this paper [2], such plants may be an adaptation to nutrient-poor conditions, where the ability to digest insects (and other small animals) would be a massive benefit, allowing carnivory to evolve rapidly.

Botanical carnivory is thought to have evolved in nutrient-poor and
  well-lit habitats such as bogs because the marginal benefits accruing
  from carnivory exceed the marginal photosynthetic costs associated
  with the maintenance of carnivorous organs.

The Egyptian mongoose is an omnivore. This species varies its diet across the year, according to what is available. For example, insects are the major component of its diet in spring, while no fish are eaten during summer (because of dry canals in the summer) and fish are a major component in the winter. This illustrates that allowing omnivory/carnivory can increase the resources available, potentially allowing better survival and reproduction relative to a herbivorous/narrow foraging strategy in the same species. Consider this problem in, for example, boreal or temperate climates, where winter can cover ground vegetation in snow and tree's will reduce foliage. Consuming animals would allow the acquisition of energy and nutrients through the winter.
In summary, carnivory can evolve because animals are a good and plentiful source of energy and nutrition, and may allow diversification of strategies, improving survival and reproduction. If animals were bad food sources then carnivory would be less common as it would be a more difficult/problematic behaviour to evolve.

While many people & organisations (including PETA) try to claim that we are not well adapted to being carnivores, many of the claimed adaptations to herbivory/lack of adaptations to omnivory are overstated, misleadingly presented, and even false, and are used in order to promote their own agenda. It's also worth noting that we are not well adapted to being herbivores (e.g. gut flora) and chimpanzees, one of our closest ancestors, are also omnivores.

[1] Krebs & Davies Behavioural Ecology, An evolutionary approach.* ISBN-10: 0865427313.
[2] Ellison, Aaron M., and Nicholas J. Gotelli. "Nitrogen availability alters the expression of carnivory in the northern pitcher plant, Sarracenia purpurea." Proc Natl Acad Sci, USA 99.7 (2002): 4409-4412.

+1, It would be great if you add the ISBN or citation for the book as a footnote instead of just providing the Amazon link. Also, please replace the journal link with pubmed/doi link as they are stable. It would be really good if you can add information from research studies on dietary/food-web models (to substantiate the lettuce-rabbit-human example). A note on evolutionary strategies would also be nice.

To illustrate the ease of digesting animals white tailed deer often eat nesting birds. http://www.bioone.org/doi/abs/10.1674/0003-0031(2000)144[0419:WTDOVP]2.0.CO;2 It is relatively easy for an herbivore to become on omivore.


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The simplest organism that can learn?
What is the simplest organism that was observed to learn: change its behavior permanently in response to some event/stimuli in a way that this change persists even if the event does not happen again?

the real problem is defining  and testing learning.

Judging from the first source brought by Bryan Krause, the definition I had in mind was associative learning.

which may be possible for even a single celled organism. Bryan Krause provided a good link to possible associative learning in amoebae.

I don't know if it is definitively the simplest, but the simplest organism with a nervous system that has been studied extensively is probably C. elegans, which is definitely able to learn.
Some basic learning abilities have also been shown in amoebae.

References:

Ardiel, E. L., & Rankin, C. H. (2010). An elegant mind: learning and
memory in Caenorhabditis elegans. Learning & Memory, 17(4), 191-201.
Saigusa, T., Tero, A., Nakagaki, T., & Kuramoto, Y. (2008). Amoebae
anticipate periodic events. Physical review letters, 100(1), 018101.


text:
Are chilies technically peppers?
Nando's chain of restaurants (UK) refers to chili peppers as just "chilies". My friend and I had a discussion with regard to whether chilies can be called "peppers" or if they do not belong to the pepper family at all. In fact, my friend added that there are 2 types of this specimen - "chilies" and "chili peppers."
To what extent is this all true, and what exactly are chilies?

Chili is a common reference to chili peppers in an abundance of countries, but they fall within the same designation as other so-called "peppers" such as bell pepper, cayenne, jalapeno, etc. because they are all of the same genus Capsicum. They differ, however, from traditional real peppers (black pepper for example) of the Piperaceae family. Capsicum actually belongs to the nightshade family (Solanaceae), but so do potatoes.
The word pepper originates from a south Indian term for the long pepper plant which was used as spice at the time and is a member of the Piperaceae family. I think that people have generalized chili as a pepper in this case due to the heat component, but this section of the answer is also off topic for this site.

All the bell peppers and chilli peppers and jalapeno's and cayenne peppers are the same species, Capsicum annuum. The bell pepper was developed in the 1920's from a hotter variety. Here are photos of the wild varieties: https://www.fataliiseeds.net/product-category/wild_chiles/ They are berries. All the american plants like tomatos and potatoes are all from the american nightshade family, Solanaceae, which evolved after America and Africa devided 180 million years ago. they are New World plants.
CKM gives you the information for paprika, a different type of plant from i.e. Sri-Lanka https://twitter.com/srilankanflora/status/773690156385644545. Black peppercorns were found stuffed in the nostrils of Ramesses II, placed there as part of the mummification rituals shortly after his death in 1213 BCE.
The only ambiguous nightshade plant which arrived before the conquest of the Americas is the datura plant, also a cousin of the pepper family, for which illustrations in indian books exist from 800 years ago, although that is a mystery and yet to be proven by DNA. If it did arrive in the old world in ancient times, then it may have arrived as seed through the Bering straights or through natural dissemination.

Chilis are from the New World, and as CMosychuk has answered, belong in the Capsicum genus. Their name derives from the Aztec Nahuatl word for the plant chilli, and this name has been used by the Aztecs to refer to the plant prior to Spanish contact and spread of the plant to the Old World.
The pepper, however, belongs to the completely unrelated Piper genus, and the plant originated in the Old World. Its etymology derives from the Sanskrit word pippali, also referring to the plant. As the Etymonline entry suggests, the word "pepper" was also used to refer to the Capsicum plants when they were first introduced to the Old World, perhaps due to their similar spicy taste.
Therefore, it is not the case that chilis are peppers, since the Capsicum genus has no recent genetic relation to the Piper genus.


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How is CO2 related to acidity in plant cells?
Why does increase in concentration of CO2 in a plant cell increase the acidity of the cell sap?
Thank you

CO2 dissolves and forms a weak acid; carbonic acid (H2CO3 <-> H+ + HCO3- <-> H+ + CO32-)

CO2 is a Lewis Acid.  CO2 is a double carbonyl carbon which is electron deficient, and we know that Lewis Acids readily accept electrons, so when present in H20 it forms carbonic acid (H2CO3).  Christiaan posted the balanced equation of the formation of the acid.

Just a comment to say the OP is talking about a plant cell; the human body's acid-base coping mechanisms don't particularly apply.

I'd say there are other just as important factors also.

@anongoodnurse thank you for pointing that out, I edited my response.  Whether in blood or xylem, CO2 will form carbonic acid in solution with water.


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What does the 'V' stand for in ECG electrode names?
In electrocardiography, electrodes have the typical names of:

RA (Right Arm)
LA (Left Arm)
RL (Right Leg)
LL (Left Leg)
V1, V2, V3, V4, V5 and V6

What does the V stand for? Is it perhaps from vector, ventricular, or maybe from something else entirely?

I would imagine it's "ventral", because they're placed on the ventral portion of the body (the front), but that's just a guess.

Short answer
V stands for voltage.
Background
The various leads in an ECG montage are shown below:

ECG electrodes. Source: American Heart Association
I am not an expert in ECGs, but as far as I can see, RA, LA and LL are return electrodes as they are situated far away from the heart. In other words, they act as reference electrodes. RL is the ground, basically to correct for baseline shifts. This leaves the V electrodes, which are the chest leads, or precordial leads, and are situated right above where the action is, i.e., the heart. The ECG is determined between the V electrodes and a distant reference, with a ground added. The V electrodes are the active electrodes, picking up the signal. The others are references and a ground only.

Thank you - I already had suspected it could be from voltage, but dismissed it, because other electrodes names are anatomy related. The limbs are in fact not all return electrodes, only the RL one is used to actively eliminate common-mode interference. The other three limb electrodes signals are there for differential measurements - they form a "triangle" of signals obtained from LA-RA,LL-RA and LL-LA.

As a paramedic who does EKGs every day, I can tell you it stands for "VECTOR" meaning the direction the electrode monitors electricity from the heart.
RA, LA, RL, and LL electrodes are ALL the principle electrodes for monitoring cardiac activity. These are referred to as the "limb leads" and are bipolar leads. The direction these leads monitor is determined by the polarity of the lead, which CAN change. For example, with Lead I the right shoulder is negative and the left shoulder is positive; but in Lead III the left shoulder is negative while the left leg is positive. Electricity flows from negative to positive. When it flows towards the positive electrode, the deflection on the EKG is upward. When it flows  away from the negative electrode the deflection on the EKG is downward.
The augmented vector leads are so-called because they have one positive electrode and the negative electrode is augmented. These are aVR, aVL and aVF where R, L and F stand for Right, Left, and Foot respectively. The V stands for vector here. In aVR, the left leg lead and left shoulder lead BOTH provide the negative pole for the EKG while the right shoulder is positive. The augmented vector leads require THREE poles to work: two negative and one positive.
The precordial leads, asked about in the original question, are UNIPOLAR leads. The computer inside the EKG uses the position of all the unipolar leads to create a "dummy" negative point at or near the center of the heart. Each Lead then becomes its own positive, and assumes that it is looking to a negative pole at the center of the heart. These are numbered V1 through V6, and the V stands for Vector. Vector 1, Vector 2, Vector 3 and so on.
One could do an 32-Lead EKG with the 3 Limb Leads, 6 Left Anterior Precordial Leads, 6 Left Posterior Leads, 6 Right Posterior Leads and 6 Left Precordial Leads. It is possible to also do a 64-Lead EKG. But the most common arrangements are 3, 4, 12, and 15 Lead EKGs.

Very likely it means Unipolar. Please note only unipolar leads aVL, aVR, aVF, and all precordial leads have the letter V. They are all unipolar. Long time ago, the "U" may have been misspeled as "V".


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Suggestion on program/algorithm to segment nuclei
I've got some images such as the one in this post, obtained from the neuroepithelium of a chick embryo in a confocal microscope, where nuclei have been fluorescently labeled. I'd like to be able to segment these nuclei, in particular to see their total area (which means I don't necessarily need them to be separated) and to count them. I tried using StarDist on Fiji, but I've obtained some very bad results, with it detecting basically no nuclei.
Does anyone have any suggestions on what I might do?
Here's a link to the original image in tif format: https://drive.google.com/file/d/1GqsUI-xnTPSKnRv_ECxJL7K785_qbq2c/view?usp=sharing
Below there's a comparison of my original image(above), with the StarDist output with low probability/score threshold and low overlap threshold (middle) and with default settings (below). Previously, default settings would output a completely black image, but it seems to have changed.

Welcome to SE Biology. It would be useful to see your best 'bad result' from StarDist and maybe a link to a tiff version of the image.

Thanks, I've edited the post with the extra information

The "Analyze Particles" function in FIJI might work.
You will run into a few problems in any entirely automated analysis because your image isn't even brightness across the image; the corners, especially the top and bottom right are substantially dimmer than the rest of the image. You might need to play with the balance of brightness to compensate in any analysis that you do. You could also cut the image into chunks and process each separately, but you might run into the problem of counting bits of the image more than once.
For the Analyze Particles function you need to

Convert your image into binary (Process>Binary>Make Binary)

Watershed (Process>Binary>Watershed); this draws lines across narrow parts of the image, creating a "watershed" (like water running off a ridge between mountains)

Analyse particles (Analyze>Analyze Particles) - play with the conditions in the pop-up window. It'll output a table with all the results, a summary page and, if you set it, an overlay window (I've shown ellipses here, but there are a few options).

I'd recommend working out the minimum size of your nuclei (I got roughly 6 pixels) and using that as the lower bound in the size setting, and working out the circularity of the objects to help get rid of small/inaccurate counts. You should also set the overlays (from the show: drop-down in the analyze particles window) - ellipses might be your most useful and comparable to the ones in your posted analysis. It will help you set the conditions for your final analysis.
I've had a go with your fairly small TIF image and it isn't great (see images above) - partly because of the resolution of the image, which is only 1 micron per pixel. If you have a higher resolution image, it should work better with a high resolution image. I got about 300 particles with min size set to 6, but this includes all the objects shown in the overlay (step 3). You might want to further filter out the smaller results manually before statistical analysis.

+1 Good answer. I've run across this need to automate counting of things (mitochondria and nuclei and synaptic boutons...) before, so often, in so many different labs. Just use FIJI/ImageJ and play around with settings and try to find parameters which are reproducible and sensible to others ( = have someone else tune the parameters independently and see if yours are similar). Surprisingly I have never heard of a better approach than FIJI. You'll have the advantage of using something open-source. Always report the parameters you set, it's good scientific practice. Good luck!

Thank you very much!! You approach gives pretty good results at first glance. The problem here seems to be that most nuclei exhibiy a "hole" in the fluorescence, which are kept by the watershed algorithm. That said, I've thought of another (more complex) way of calculating this and will be comparing both methods! I'll be trying to obtain better images of course, but this was a first approach to the problem. Thanks again for your trouble!

@SantiagoBosch I noticed the holes in the nuclei and tried the Process>Binary>Fill Holes option, but it just combines all the nuclei that overlap in the middle of the image, and it doesn't work after watershed. You could try really increasing the brightness + contrast of the red image (Image>Adjust>Brightness+Contrast), then process to binary, but I don't know if that will work either.

@SPr I guess because IJ/FIJI have been designed for scientists by scientists working on the same problems as us, and it is free + open source, it makes it an ideal tool, and someone will have come across your application or something similar in the past and worked out a solution. You can also automate most of the processing using IJ fairly simply (as you can in photoshop etc) if you care to learn a little bit of programming in Macro or Java.

Fiji have a machine learning segmentation utility (WEKA). it's simple to train and use.

@heracho That sounds like the beginning of an answer - we welcome additional answers here so long as the answer the question, and I'd love a better solution than mine as it is definitely flawed

I'd really urge you to look into machine learning for this task.
You can probably get away with classical image analysis for an 80/20 solution on a particular image set, but it will be a lot of work getting there and it probably won't generalize very well.
In particular, I've had good success even for difficult cases (eg where nuclei touch or where only a subset of nuclei were to be counted) with U-Net based segmentation: In such cases, to count nuclei, I've trained U-Nets not really to segment but to place a dot on each nucleus.
Counting dots you get a very good approximation of nucleus count.
See here for details.
In order to get area, shape, intensity... as well, it can be useful to train an algorithm to segment an image into three classes: background, object (nucleus), and border.  This way, you'll mitigate the problem of touching regions which makes it difficult to tell apart different objects in the segmented image (see here).
Oh, and there are plenty of solutions out there, these days, for training machine learning algorithms without having to know much about how they work.
Full disclosure: I'm one of the developers of one of these solutions, VAIDR.


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Method to detect Protein aggregation
I have a specific human protein that was purified from E. coli.

This protein was tagged with MBP and diluted in an elution buffer.
This protein has a tendency to aggregate, and when it does, it can induce the nearest protein to be aggregated too.
We believe that tagging MBP prevents this protein from aggregating, so that when MBP is cut off from the protein, it will easily aggregate.
I want to confirm this. However, I am not sure how to check if the protein is aggregating or not.

I would like to know whether my protein is aggregated, what is the best method to detect protein aggregation?. I would really appreciate if anyone can give me the reference or protocol.

What do you mean by "my protein is aggregated"? In a sample preparation? In cells?

Welcome to SE Biology. We are happy to try to assist people with biological problems, but we can only do that if we know what the problem is. So, first, please finish reading the [Tour] (we know you haven’t) and then read the Help on asking good questions. You are so close to your own problem that you think more experienced scientists must know what it’s all about. We haven’t a clue! What is your protein? Is it pure, in a mixture, in a cell or what? Why do you think it might be aggregated? Tell us what you are doing and what you observe. Only then can we help you

Thank you so much.  Let me provide some background: I have a specific type of human protein that was purified from E. coli. This protein was tagged with MBP and diluted in an elution buffer. This protein has a tendency to aggregate, and when it does, it can induce the nearest protein to be aggregated too. We believe that tagging MBP prevents this protein from aggregating, so that when MBP is cut off from the protein, it will easily aggregate. I want to confirm this. However, I am not sure how to check if the protein is aggregating or not.  If anyone has any suggestions, please let me know.

@Sketsawy you need to tag people with the "@" to let them know that you are talking to them. Also, the information that you've provided in your comment would be very helpful included directly in the question, so I'm going to edit your question to include it there.

I started writing a comment but it got out of hand so I'm just doing an answer.
There are many many papers that describe methods for detecting aggregation. Below is a semi-random sample.
What exactly is the roadblock that you are encountering? Which of these kinds of methods have you tried? Are you working in live cells or only in vitro? Are you open to putting your protein into yeast?

Removing MBP tags from proteins
Methods in pharma for detecting aggregation (older).
Methods in biomanufacturing for detecting/managing aggregation.
Papers with informative methods sections for testing aggregation (mostly in yeast, which is probably the easiest system for studying prions):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6980781/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6980676/

https://www.sciencedirect.com/science/article/pii/S0076687906120121

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066306/

https://www.sciencedirect.com/science/article/pii/S1046202306000594

Visualizing aggregates in live cells
Microscopy of aggregates in live cells