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Species Identification: Small white maggot/larvae, Missouri USA
I'll try to give as much information as I can, because I don't know which information will be more important.
We woke up this morning to these little white worm/larvae in the house. We are located in the northern portion of southeast Missouri. We live next to some horses and cows. We have 1 inside dog and 1 outside dog. I'd say more of the worms were found in the kitchen (Tile floor) but some were also found in the living room (Hardwood floor).
This is a side view of the worm.
This is a perspective view of the worm. (About a 1/2 inch long)

It's the larvae of an insect - probably a house fly/bluebottle (it looks very similar to the typed used for/bought from fishing suppliers as "maggots")

Try to keep it in a jar and see if becomes an adult, that will be easier to ID.

We've kept one to the side. We'll see what happens. We've also called a pest control in our area to come and look to see what they think about the situation.

What ever became of the specimen you kept? Any adult pictures?

I kept some in a jar, but they all turned hard and brown. I assumed they died. I left them for a while just in case, but they never did anything. I'm kinda hoping they come back. I want to try again!


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Species Identification: large shiny black beetle, Detroit USA

What sort of beetle is this? I live in a suburb of Detroit and found a whole bunch of these living under my lawn when I was replacing a section of it. I'm assuming these are also the source of the grubs I found as well. Are these harmful?

You found a stag beetle (family Lucanidae).
Although the males are much more readily recognized with their large "stag antler" shaped mandibles, these species are often sexually dimorphic with females having much smaller mandibles (e.g., see here). However, in some species the males' mandibles are likewise diminished and not stag shaped.
According to the Wikipedia page:

Currently, the only means of identification of world species is the illustrated text by Mizunuma, T. and S. Nagai. 1994. The Lucanid Beetles of the World. Mushi-sha, Tokyo. 337 pp. based on the work Catalogue illustré des lucanides du globe in Encyclopédie Entomologique (series A 27: 1-223) by Robert Didier and Eugene Seguy.

So without this guide (and without known dimensions of your specimen), an exact identification will be very difficult.
However, your species looks very similar to a male specimen of Lucanus placidus.

Additional pictures (such as the one below) can be found here.

According to Wikipedia, L placidus is 22–35 mm long, has two or more teeth on its jaws and has dark femora. The species is sometimes found in soil and it does live in Michigan:

We can rule out Lucanus capreolus because the color is wrong:

[L. capreolus is] dark reddish brown in color with a smooth, shiny elytra; [their] femora are orange-brown.

It's a Lucanus. Don't know the concrete species.

It is not clear to me that the two insects are in fact from the same genus, since the Wikipedia stag beetle has much larger mandibles than the one pictured.

@MarchHo Mandible size varies between male and female, and between species in the genus, so it might be a type of lucanus. That said, this answer is probably more appropriate as a comment until something more definitive can be provided.

So, after all, it can really be a Lucanus, so why the downvote ? For a new user like me, it's very discouraging to get one.

A downvote just means the answer isn't useful. You haven't provided any evidence to support your answer at present. I'd suggest adding what key you used and ideally a pointer to some resources that would allow the OP to follow it up to species level (or if it's too difficult to go to species level, why it's too difficult). For what it's worth I think you're right about it being Lucanus (probably capreolus). Please check out the tour for advice on how to write a good answer. And welcome to Biology.SE!

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How do cells age and die if they are dividing into new cells?
If cells in our body keep on dividing into new cells how do they ever grow old?
The only cells to grow old would be defunct cells or those who won't divide into new cells like nerve cells.
What am I missing here?

Human chromosomes contain certain DNA regions called telomeres. These regions are shortened on each cell division and once they are gone, the cell cannot divide. Therefore an average cell in our body can divide only about 50 times.
There are indications that longer telomeres may increase lifespan, however this remains controversial. Telomeres are believed to be a method of higher organisms to prevent uncontrolled cell division and cancer, therefore artificially increasing telomere length may not lengthen but shorten lifespan because of increased cancer risks.
Also, ageing is not (only) caused by individual cells growing old. Often it is the organization between the cells that breaks down. Scarring is a good example for this. The wound is closed but the tissue inside the wound was not able to organize into functional skin tissue again but rather "patched up" the wound with comparatively unorganized tissue.
The brain is another extreme example of ageing by disorganization. It has been shown that even adult brains contain neuron progenitor cells (albeit fewer than other tissues) so even adults can regrow neurons in the brain. However, while the cell body of the neuron can be replaced, all its (sometimes thousands) of connections to other neurons are lost. Therefore, brain tissue can be regenerated in principle, but the information it contained cannot.

That makes it like a chicken and egg problem if division is limited then how do new cells form to take place of dead ones?

50 divisions per cell is plenty. That is a limit of 2^50 cells, which is tons of biomass. The cells that take the place of dead ones are called stem cells. They are spread throughout every tissue and are still able to divide and differentiate.

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Using exogenous genes to reduce the set of essential amino acids?
Various organisms have sets of essential amino acids that they cannot synthesize themselves, but rather that they must obtain from food. Humans have 9 of these amino acids. However, obviously certain organisms like plants contain the necessary genes to synthesize all of their amino acids. Also, the set of amino acids for various organisms differs. For example, arginine is essential in dogs but not in humans.
Have there been any attempts at taking cells from an animal or other organism with essential amino acids and providing them with the necessary genes to synthesize that amino acid, thereby reducing the cell's set of essential amino acids?
I am not asking this specifically referring to human cells, nor do I have any particular motivation for asking this other than curiosity.

Decreasing the number of essential amino acids is frequently used as a selection marker during molecular biology experiments: An organism (usually yeast) that cannot synthesize a certain amino acid is first grown in the presence of said amino acid in the media. Then it is transfected with a gene of interest together with the gene that enables it to synthesize the amino acid. Now being grown in a culture medium that does not contain the amino acid, only individuals that were successfully transfected can grow, the others will starve.
A similar approach was also used in  Beadle and Tatum's Nobel prize-winning work on the one gene-one enzyme hypothesis.


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Species Identification: Red velvety insect, India
What species is this?

Description:

Location: India
These insects came out just after overnight rain.
They were all over the place.
Their body looks like velvet.

Are these insects poisonous?

As you might have noticed from its appearance, this is a red velvet mite. This is an arachnid (related to spiders) and not an insect.
The red velvet mite apparently does not bite or sting (according to this website), and it is also used for medicinal purposes in India, according to this Wikipedia image, so it is unlikely to be dangerous.

If you haven't seen it already, the webcomic The Oatmeal has an amusing take on some of the arthropod's mating habits.

+1 for factually correct, complete answer (with Oatmeal link). A bit more detail on those 'medicinal purposes': "the inhabitants of Chhattisgarh use this mite (in combination with other herbal drugs) for the treatment of more than 10 important diseases including malaria, urinogenital disorders, paralysis, etc. Its use as sexual stimulant is most popular in the region".

I've noticed that whenever the locals believe fill-in-the-blank random plant/animal/insect/etc cures like 35 diseases and ailments and also bestows epic boners, chances are it does nothing.


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Why are vaccines for polio taken orally while vaccines for TB need to be injected?
My thoughts are that maybe the TB antigens necessary to produce an immune response are proteins; therefore they can be digested in the stomach and small intestine. But I may be wrong though. I am confused why I can't say the same for polio vaccine.

There are different polio vaccines - one live (attenuated) vaccine which is given orally and one inactivated, which is injected. The main reason for using the live orally vaccine is that it provides excellent immunity (better than the inactivated) since it uses the natural infection route (oral-faecal) in the body where it enters through cells in the intestine. Besides that, it is also much less expensive than the inactivated form, which is a big thing when doing mass immunisations in developing countries.
The live vaccine, however, may mutate back into a more infectious form as you shed live (attenuated) viruses after the immunisation, so these are not used anymore. Now we are very close to the eradication of the poliovirus. The risk of getting new infections is viewed as being too high these days. See this paper for more information: "Vaccine-derived polioviruses and the endgame strategy for global polio eradication."

Also the injected vaccine often does not stop someone getting infected with polo and passing it on, it "just" stops the person getting ill from polo.

@IanRingrose can you explain your claim, preferably with citations? A vaccine (any vaccine) is meant to stimulate the immune system so it can quickly destroy the infectious agent when it is encountered. "Passing on" a disease means it has taken hold in your body in sufficient amounts that others can be exposed to it, that's what the word "infectious" means. Vaccines stop that transmission.

@MattDMo,  Polio is spread by getting into someone’s stomach and coming out of the other end, but needs to get into someone blood to make them ill,   The injected vaccine quickly gives a good level of immunity from white blood cells; however it produces very low levels of immunity in the intestine.  (As a result, when a person immunized with IPV is infected with wild poliovirus, the virus can still multiply inside the intestines and be shed in the faeces, risking continued circulation) see http://www.polioeradication.org/Polioandprevention/Thevaccines/Inactivatedpoliovaccine%28IPV%29.aspx

There are also different types of the oral vaccine, as there are 3 types of polio can including all 3 in the vaccine make it less effective, see http://www.polioeradication.org/Polioandprevention/Thevaccines.aspx

It comes down to a choose between the vaccine that gives the best protection for the person getting given the vaccine, and the vaccine that is best at stopping ANYONE from getting polo, by stopping polo spreading.

@IanRingrose thanks for that! I forgot about injected vaccines not being very good at stimulating mucosal immunity.

The reason why the oral polio vaccine is not digested in the stomach is that the poliovirus itself has adapted such that it can survive the acidic conditions of the stomach. By using an attenuated (mutated to not cause neurological symptoms) version of the virus, the oral vaccine can also survive the acidic conditions of the stomach. For TB which is transmitted not through ingestion but through inhalation, the bacterium is not resistive to the stomach acid and therefore a different vaccination strategy had to be used which requires injection (which, as described in the answer by Chris, is also less dangerous).

Note that rotavirus vaccine, given to infants, is also given orally, and it too is a GI tract infection.  We think of polio as affecting the nerves, but that's a weird exceptional outcome, it's usually a stomach bug.  So when we expect the primary infection to happen in the gut, that's where we prime the immune system.

A point to note that TB is cause by a bacterium and not virus as you've written "the virus is not resistive to the stomach acid..."

Also note that breastmilk, while not a vaccine, does contain antibodies, and those do work to reduce the rate of GI illness.  So there is an immune system working in the gut, and it can be affected by vaccines and antibodies given orally, they don't get digested before they have a protective effect.

@ABcDexter, Thanks, I corrected the answer accordingly.

@swbarnes2 This may be true for newborns but certainly not for adults. All antibody based treatments are given intravenously (see also monoclonal antibody therapy).

As stated by others, polio is primarily a gastro bug, an enterovirus related to Coxsackie and a number of others which produce stomach and respiratory symptoms, as well as various others.
Most polio infections result in nothing worse than a case of "the stomach flu", but in a small percentage of cases the virus escapes from the GI tract and produces neurological symptoms.  And in a small percentage of those there is the paralysis that people associate with polio.
Since the route of infection is primarily oral, a live (but "attenuated") polio virus can be administered orally to achieve immunity to the "real" virus.  Other diseases are either not spread orally or they do not have live-attenuated vaccines that have been developed.  Simply administering the antigens orally would not work, as they would be too dilute and would be quickly neutralized by digestive juices.


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Electron balance for biomass synthesis: is my professor right?
I'm studying for my exam and I came across these notes written by the professor himself. He's talking about the general reaction of biomass production in a bioreactor:
$$\ce{C6H12O6 + NH4+ + O2 -> $\mathrm{C_wH_xO_yN_z}$ + CO2 + H2O + H+}
\\\text{(not balanced)}$$
At some point he proceeds to do the "reduction balance" for this reaction: he calculates the "reduction degree" of the elements (which he defines the same way I define the oxidation number) and here comes the problem.
He states the "reduction degree" of C in glucose is +4 and the one of O in O2 is -2.
Is "reduction degree" different from oxidation number? Are there any particular ways to calculate oxidation numbers when you talk about biomass?
Thank you for your help.

The terms are different.
Oxidation number is the difference in number of electrons (not pairs) from the elemental form (which for many elements exists only on paper) of an atom.
Degree of reduction is a more uncommon term that is basically the number of electrons that atoms in a molecule are donating per atoms of a given element. It is calculated formally by summing the number of electrons donated to reach a full shell (H=1, C=4, N=-3, O=-2, P=5, S=6 etc.) divided by the number of a given element, but that is more confusing than anything.
Carbon can be oxidised four times, e.g. methane > methanol > formaldehyde > formate > carbon dioxide (not biological route, just an example), while oxygen can be reduced twice: to hydrogen peroxide and then to water. As proof, most O2 dependent enzymes produce hydrogen peroxide (e.g. FADH2 enzymes). That is a cheat way to work out where those numbers come from.
I would recommend forgetting about the formal calculations of oxidation numbers —in biology oxidation numbers of carbon are generally not discussed.
I will open the brief parenthesis of the oxidation states of carbon just to point out they are not those: -1 for a bond with hydrogen, +1 with oxygen and 0 for a C-C bond. Carbon monoxide therefore has an oxidation state of +4, while a C in glucose (on average) has a -1. Molecular oxygen has two identical atoms therefore is 0. Elemental carbon has 6 electrons so hypothetically you cannot strip carbon more than +6.
Here what is important is figuring out how many times a carbon in a molecule can be oxidised, that is how many electron pairs a molecule can give away as every time that happens an NAD+ (catabolism) or NADP+ (anabolism) is reduced, which is key to the cell. A dehydratase removes a hydroxyl group leaving an alkene, but it does not carry out a redox reaction: the geometry is no longer sp3, but sp2, and the oxidation state has decrease by 1 in that carbon, yet carbon kept its electrons —the other carbon increased by 1 as it deprotonated, so no net change and NADH is not generated.
Knowing how many electron pairs are given away going from glucose to carbon dioxide is important because cells cannot make them disappear and a terminal electron acceptor is needed either in the form of respiration or fermentation. There is a further concept, that of reduction potential. Different forms of terminal electron acceptors are employed in Nature: oxygen, Fe(III), sulfate etc. and these have different "energy" levels at which they accept the electrons (reduction potential, measured in volts), which translated to different amounts of energy that can be syphoned off during the reaction.

I don't think you answered the question --- what is "reduction degree", and is it different from oxidation number / oxidation state? You mention "redox potential", by this do you mean "reduction degree"?

Sorry, you are right. I edited my answer.

Thanks, it is improving!  Can you provide some references on "degree of reduction" ?  This seems like a pretty obscure concept --- I teach cell biology / biochemistry but I have never heard about this, and I have a hard time finding anything.

Sorry, after staring at this for some time, I still don't get your definition of "degree of reduction". What do you mean by "divided by the number of a given element" ?  Atom number?  Stoichiometry coefficient?  As I understand it, you should multiply the atom valence by the stoichiometry coefficient ?

I also didn't quite get how you determine the reduction degree..
For example: I can follow you when you talk about different oxidation states of carbon, but still I don't get: what is the reduction degree of carbon in glucose and carbon dioxide?

The crux of what I tried to say is to not concentrate on the maths and to focus on the concept that the more the carbon is bonded with oxygen and less with hydrogen, the more electron pairs the molecule gives away (= oxidised). Hydrogen is happy as a proton, not a hydride. If the latter were true all of this would be meaningless. Instead you have to have NADH carrying the hydride (and the energy with it).


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Why do people remove excess solution after they put on a coverslip?
Today, my classmate and I stained a slide of cheek cells. After we put on a coverslip, our teacher said that we are supposed to remove excess solution using a tissue.
Why should we do this? I am so confused

If I understood the question, it's just because otherwise the solution would flow out and stain the microscope.

If you leave it is messy, it can obscure the image when the stuff is on top of your sample, if it sticks to the sides the slip may float on it. If you press the slip slightly you push out bubbles and excess liquid. then by carefully removing any excess fluid you will get a stably fixated slip on a clean prep that is ready to watch.

Well, from personal experience, whenever there was excess solution on the glass slide, our teacher always commented that our slides were messy. So I guess the entire idea is to keep the slide neat, clean and to make it look presentable for observation. Also, in case the excess solution flows out to the entire surface of the glass slide, the stage clips may not be able to hold the slide in place when it is kept on the stage of the microscope (since it would be all slippery). Usually, only such little things go wrong, nothing huge. It is actually more of a basic etiquette or precaution that is followed while preparing a slide, like wiping your mouth after eating. Your observation is not affected in any way.

Neither of the current answers fully answer the question.
The amount of liquid underneath a coverslip should be just sufficient to hold the coverslip and sample onto the slide. If there is too much water, the surface tension would become reduced, allowing the coverslip to fall off the slide.
Additionally, minimising the amount of water between the coverslip and the slide would ensure that the z-axis variation in your sample is minimised, therefore reducing the likelihood that your sample will have different focal points across the sample.
This UCLA guide on microscopy slide mounting explains it (emphasis mine):

Small pieces of filter paper (Whatman #1) are placed around the edge of the coverslip to absorb excess mounting medium. If your specimen is tissue culture cells or frozen tissue sections, this should not harm them. This does two things: a) it allows the coverslip to come as close to the specimen as possible and reduces the depth of the field. You will get less focus aberration if you do this judiciously. b) the coverslip will be a lot less likely to float around on the slide and move which could specimen damage. The surface tension between the coverslip and slide will be much higher. You will also be much better able to seal your coverslip to the slide.

March Ho is right: when viewed at any magnification, that tiny amount of fluid between slide and coverslip is an ocean, where all those things are present that are present... well in an ocean: fluid currents and those critters once just underneath the surface, than again "in the deep". As March put the later: "z-axis variation".
Those involved in studying live critters, pond dipping and such (everyone should do it at least a few times!) know the phenomenon all too well.


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Which diagram correctly describe an effect of tar entering lungs?
Which flow diagram correctly describes the effect of tar entering lungs?

Tar is a cause of Chronic obstructive pulmonary disease (COPD) which includes both chronic bronchitis and emphysema and it is also a carcinogen, too. So, I think that A, B, and C would be correct answers, but the solution is A. Why B and C are incorrect?
Thank you very much!

COPD is not caused by an infection (which would require a pathogen) but by the inflammation reaction the body triggers because of the tar particles. Thus the statement "mucus accumulated causing infection" does not correctly describe the effect of tar on the lung. Consequently, B and C are incorrect.


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How many cell membranes are oxygen and carbon dioxide diffuse through in the lungs?
In the lungs, oxygen and carbon dioxide pass through cell membranes by diffusion.
Which row is correct?

The correct answer is D, but I think it should be B. I can only think about three layers as maximum which are; epithelium of alveolus, endothelium of capillaries and the membrane of red blood cell. I don't know what are remainings.
Any help would be much appreciated!

Assuming that user24284 /Jam's answer is the correct way to think about it (I think it is), the question is a bit ambiguous. We don't know where to stop: should we track O2 until it reaches blood? or the final destination cells (where O2 is actually consumed)? In the latter case, the correct answer is not actually more than 5, since the oxygen also has to exit the erythrocyte (+1), enter the destination cell (+1), cross mitochondrial membranes...

This looks like a homework question.

Oxigen goes from the alveolar's lumen to the cytoplasm of the erythrocyte, and that's 5 membranes:

the "top" of the alveolar epithelial cell
the "bottom" of such cell
the "top" of the endothelial cell (capillary)
the "bottom" of such cell
the erythrocyte membrane

You got all the cells right, but your only problem was this: oxygen diffuses through the cell membrane entering the cell, moves through the cytoplasm, and diffuses through the membrane again exiting the cell. So, for each cell, you have to count 2 membranes. For the last one, the erythrocyte, you have only 1 membrane (because it is $\ce{O2}$ final destination).
For the $\ce{CO2}$ the situation is a little bit more tricky. We have the same 4 membranes (2x epithelial cell and 2x capillary), but $\ce{CO2}$ can come from 2 locations:

from the erythrocyte, where it is formed from $\ce{H2CO3}$ (by the reaction $\ce{H2CO3 -> H2O + CO2}$) or released from the N-terminal group of proteins, like haemoglobin (where it has previously bound)
from the plasma (around 9% of the $\ce{CO2}$).

In the first case we have 5 membranes, and in the second case just 4.
So, the correct answer is D.


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How would one determine if an up regulation of one protein leads to an over expression of another?
Again, I'm new to biology and have a bunch of questions.
Does it depend on the proteins involved? OR are there basic co expression procedures one could implement to determine exactly how much one protein upregulation leads to overexpression of another protein ?

It might depend on what protein you are studying.

To demonstrate a causal relationship where protein A leads to increase in protein B, you need to experimentally increase the level of A and measure if B increases. Over-expression is typically done with overexpression of protein A from a plasmid containing the coding sequence, driven by a strong promoter that causes high levels of protein synthesis. See this Wikipedia page for some pointers. Relative protein levels can be quantified by western blotting. The experimental details depend a lot on what cell type and protein you are studying, of course.


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Fine permanent fluorescent marker for blue light
I am looking for a fine- (or small-)tipped permanent marker to write on Petri dishes that is visible under a blue light or a transilluminator. It would seem obvious, but it is a nuisance.

The Sharpie Neon series are too thick.
Highlighters and all the arts pens I have tried rub off the polycarbonate.
The red colour from Staedtler lumocolor (black body) shows up faintly —none of the other do— but too faintly.
The Neon series from Staedtler triplus fineliner (gray body, triangular) rub off

So I would like to find what solutions other have come up with or if there is a brand that works well.
EDIT. This is how the Sharpie series look:

I have had this problem before... this is what I ended up using:
https://www.amazon.com/Invisible-Blacklight-Marker-Blue-Yellow/dp/B004C89M9Q
You may have to write on a tape or something so that the ink doesn't come off. (Ink may come off if you incubate plates)


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Mesoderm vs Mesenchyme- what's the difference?
My embryology textbook states that mesoderm can exist as Mesenchyme or Epithelium. I'm not sure what 'epithelium' means. Here is a quote for context:

Somatic, splanchnic, and somite mesoderm can be temporarily an epithelium.
  The temporary epithelium transforms to a secondary mesenchyme

What does this quote mean?

Mesenchyme is the meshwork of embryonic connective tissue in the mesoderm; from it are formed the connective tissues of the body as well as blood vessels and lymph vessels.
So it's a part of mesoderm

Welcome to BiologySE...thanks for taking a stab at this answer. We always appreciate some references/links for answers so other users can read more about your answer. It will definitely help the strength of your answer as well.


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The Perplexing Trilobite: What is the Evidence Supporting The Hypothesis That They are Not Crustaceans?
In the field of paleontology, one question that's really bugged me (er, no pun intended) of late is why the subphylum/class Trilobitomorpha/Trilobita is off on its own branch of the Arthropoda phylum, or alternatively should be slotted under the Mandibulata clade.
What is the evidence justifying these hypotheses?
From a layman's perspective it seems compelling both from what is known of the physiology and morphology that it would make more sense to tentatively classify them as a early member of the order Isopoda, a part of the subphylum Crustacea.
Indeed, Alex Chestnut's Master's dissertation, "Using MORPHOMETRICS, Phylogenetic Systematics and Parsimony Analysis to Gain Insight into the Evolutionary Affinities of the Calymenidae Trilobita" states on the history of trilobite studies that Charles Lyttleton, one of the earliest documented discoverers of trilobite species, asserted that trilobites belong not to insects, but to "the crustaceous tribe of animals."
Indeed, if this is the case, morphologically we see that the trilobite shares many features with modern isopods (i.e. "sow bugs", "pill beetles", "roly-polys" etc.).  Look at this newly discovered albino cave isopod, for instance:

And now look at this fossilized Crotalocephalus africanus:

And this Armadillium vulgare (Latreille) pillbug:

And this Crotalocephalus trilobite:

Well, you get the idea.  Trilobites look perhaps look morphologically more like isopods than any other living order (although a certain roach (members of the Laxta genus, i.e. Laxta friedmani) does also look uncannily similar until you get to the legs and wings).
And apparently at one time, they were classed under Crustacea (the subphylum Isopoda is in), hence raising the possibility that Isopoda may be "living fossils" or the modern descendants of trilobites.
However, the Wikipedia entry for trilobites states:

Once soft-part anatomy had been recovered, the trilobites were
  originally allied to the Crustacea; however, this suggestion has since
  fallen out of favour.

While it goes in depth into what is known or believed to be known about trilobite physiology and morphology, it never really explains WHY trilobites are no longer believed to be crustaceans.
It goes on to state, though, that apparently this is being reconsidered... but not in the subphylum Chelicerata (?!) which Isopoda lies under:

A relationship with the Chelicerata, in a clade termed Arachnomorpha
  (Arachnata), was in vogue for some time; a position in the Mandibulata
  (=Myriapoda + Crustacea + Hexapoda) stem-group may be a more
  parsimonious alternative.

Ugh, Myriapoda?  Why?
First, members of Myriapoda generally have simple eye structure, where as members of Crustacea typically have compound eyes.  Trilobites have compound eyes!
Now the other defining characteristic of crustaceans vs. myriapods, from what I've read, is the brain size.  But from what I understand little is known about the trilobite brain.  But I would argue the presence of compound eyes and the believed predatory niche suggests a more complex brain.  So that would make another somewhat hypothetical reason to pick Crustacea over Myriapoda.
I was unable to identify any clear evidence in favor placing trilobites in Myriapoda vs. Crustacea..
Let's look at the overall defining morphological/physiological traits of Crustacea:

Three body regions -- head, thorax, and abdomen (possibly fused).
Exoskeleton is typically hard and molted
Each somite (body segment) can have a pair of appendages which "vary widely"
Abdomen bears pleopods (swimming legs)
Appendages are often biramous.
Open circulatory system Straight digestive track
Brain and kidney structures near the antenna
Eggs hatch as larvae

To my knowledge other than the internal organs (which are not well known) trilobites meet all of these criteria.
And then there's the visual test, as seen above, between living isopods and trilobite fossils.  They look obviously similar.
According to the chapter "The Trilobite Body" in Kaesler, R. L.'s, "Treatise on Invertebrate Paleontology, Part O, Arthropoda 1, Trilobita, revised. Volume 1: Introduction, Order Agnostida, Order Redlichiida", each endopodite (walking leg) had 6 or 7 segments.  This might appear to be a morphological difference between modern isopods, but it is also stated that basically ALL early arthropods (including early Crustacea) are known to have this segmentation.
That brings me to my final point ... whatever scant few traits that do offer some evidence against trilobites being an early member of Isopoda in the Crustacea subphylum appear to be in part, at least, morphological differences that are somewhat ambiguous and may be merely evolutionary artifacts that existed in other Crustacea at the time as well.
So the visual and morphological evidence seems to point strongly to trilobites being isopods.  What compelling evidence exists in favor of putting them under the subphylum Chelicerata?
And why is that evidence viewed as stronger than the aforementioned evidence to put it under the subphylum Crustacea, perhaps as early ancestors of Isopoda.

This question is really long and would benefit greatly from being far more concise

Fair enough @rg255.  I've deleted the first paragraph as it was overly conversational and not overly pertinent.  Do you see anything else that should be removed?  Most of the text appears necessary as I'm outlining the morphological basis for classification, the history, etc. in order to illustrate the evidence to the contrary of the hypothesis I'm asking the justification of.  That allows me to ask the additional later question of why whatever evidence does support the hypothesis is thought to be greater than the aforementioned evidence supporting the Isopoda phylogeny hypothesis.

It is still pretty long and I am personally way too lazy to read it :). Splitting the questions into semantics parts (using section titles) and avoiding redundancy should help. Smaller pictures may make the post less intimidating too.

Trilobites had bodies divided into 3 lobes lengthwise.  Hence the name trilobite = 3-lobed critter.  The head or cephalon of the trilobite is large, nearly as broad as the body and marked by sutures.  These are the easy-to-see differences.  There are several other differences that it would typically take a trained paleontologist to detect, including crystaline calcite lenses in the eyes, a rostral plate, and hypostomal wings.  These are summarized here with nice illustrations: http://www.trilobites.info/triloclass.htm#trilobites.  More details:  http://www.trilobites.us/trilobite-morphology.htm.
The overall similarity between isopods & trilobites may be due to convergent evolution, isopods replaced trilobites in a benthic detritovore niche after the great Permian extinction.  https://en.wikipedia.org/wiki/Permian%E2%80%93Triassic_extinction_event
Claiming that "isopods are trilobites" appears to be the first new argument from the creationists in a century.  https://sciencenotes.wordpress.com/2006/04/29/trilobites-are-not-isopods/
explains and has a prettier isopod picture.


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If crocodiles are k-selected, why do they supposedly "not age," as in avoid senescence?
I recently saw a few sources stating that Crocodiles do not biologically age, implying negligible senescence. Basically, a 70 year old crocodile is in the same physical/health condition as a 7 year old crocodile. However, crocodiles are K-selected, meaning that populations are generally close to their carrying capacity. If they do not exhibit natural senescence, isn't that evolutionarily disadvantageous, because the younger crocodiles with more slightly more fit genes will not necessarily replace the older generations, meaning that crocodile populations would adapt to environmental changes significantly slowly. Can someone please explain to me how this lack of senescence can apply for this type of species?

Your premise is almost certainly wrong.  As a rule of thumb, virtually every popular account that claims certain animals don't age is bullshit. Unless you have a peer-reviewed paper that explicitly states the animals doesn't undergo senescence, assume that it does. In this case this paper offers an unconfirmed claim that old crocodiles are senescent.

Comments
You seem to use the term evolutionary advantageous vs disadvantageous for the species rather than for individuals. It is a very common misconception from the general public. You might want to follow an introductory course to evolutionary biology such as Understanding Evolution (UC Berkeley) for example.

younger crocodiles with more slightly more fit genes

"fit genes" does not mean much. Again an introductory course to evolutionary biology should help you there.
Answer
You'd right though that absence of senescence causes longer generation time and therefore lower response to selection pressure (such as those caused by an environmental change). But populations don't evolve in order to maximize the probability of the survival of this population (related to first comment above).
Those that live longer, leave more offspring and therefore long-lived individuals are expected to dominate the population in the long run. The evolution of senescence is not exactly that easy though otherwise no species would show any sign of senescence (see Why does evolution not make our life longer?).

Sorry, I'm a bit confused on two things. Firstly, for the younger generation being fitter, doesn't that generally apply in times of selective pressure? In this case, the slightly more fit individuals will reproduce a bit more and thus, more offspring will carry on those genes.    And also, during selective pressure, more fit individuals will reproduce, so generally the alleles for the more advantageous genes will appear in higher frequencies, causing the population to adapt to environmental stresses.

Yes, you are right, the expected the change in population mean fitness is increasing by the value of the additive genetic variance in the previous generation. Of course, it is only the expectation from a distribution. I removed this small piece of sentence.

The main point is that you seem to think that what is increases the probability of a population to survive should be selected for while this is not what natural selection does.

So as of crocodiles, they have been able to maintain the negligible senescence due to a lack of selective pressures? Otherwise, crocodilian populations would have lower responses to environmental stresses.

It is possible that an eventual quasi-absence of external causes of mortality (such as predation and parasitism) would remove the interaction between age and reproductive success resulting in more efficient elimination of old-age deleterious mutations. I realize I might use concepts you could be unaware of here. I would strongly recommend that you read Why does evolution not make our life longer?, you will like this post!


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Species Identification: Waterborne larvae, Texas USA
Can you help identify this worm?
It was found in a cup of water at a restaurant (unpleasant, yes), likely came through the water system. (Location: Texas)
Found these images of it online (in which they were also found in water systems - dog bowl, sink), but none of the sites identified it.
Significant features: black head, black pointed tail, clear body with grayish intestines visible, tiny (2-3 mm)
Similar larvae that don't match:
-Mosquito larvae
-Midge larvae
Any insight is appreciated, including if you are familiar with similar looking larvae. Thank you.

The larvae are moth flies (Psychoda sp.)

The black head, black pointed tail, clear body with grayish intestines visible and also their small size 2-3 mm can be seen on both pictures.
Where they can be found in nature:

In nature, moth fly larvae, Psychoda sp. (Diptera: Psychodidae) normally occur in aquatic habitats that experience intermittent submersion or flooding. The larvae develop in polluted, shallow water or highly moist organic solids where they feed on decaying organic material in mud, moss or water.

Where they can be found in households:

In homes, the adult flies, which resemble tiny moths, are most likely found on the walls of bathrooms, kitchens, basements and other locations where sewer drains and plumbing fixtures are located. The flies are poor fliers and usually are found close to the drain or area from which they came. Moth fly larvae are known to live in drain traps, garbage disposals, toilet tanks, sides of drain pipes and overflow pipes in homes, wet areas around leaky pipes, sewer lines, and septic tanks where they feed on stuff that might accumulate in such areas. The moth flies that live in Michigan do not bite and are not known to transmit disease of any sort.

What to do against them:

The best way to control moth flies is to eliminate or reduce the larval food sources by thoroughly cleaning drain lines and plumbing fixtures. Pouring boiling water down the drain where larvae are suspected to be may help to reduce their numbers. Adults can be controlled with the application of a household aerosol insecticide (like Raid) or a good flyswatter. Be sure to read and follow all instructions and safety precautions found on the label before.

There are various other methods which are far more precise, listing how to eliminate moth flies from drains.

But what happens if someone drinks them along with water?

@rishabbairagi I suppose that your stomach acid can deal with them, worst case scenario would be internal myiasis which could cause cramps, vomiting and diarrhea,.

@JordiZambrino My concern is that the article you quote only says they are found near dirty water, nothing you'd want you to drink. If your drinking water is full of maggots, what other pathogens are floating around in that?

@user137 Pathogens that would be floating around in drinking water; I'd suggest they could be MSSA and MRSA Staphylococcus aureus

These are moth fly larvae (Psychodidae). They live in sinks, bathtubs etc. See
http://bugguide.net/node/view/201443/bgimage

Please include an image that shows this is the right ID, as well as additional supportive evidence, such as that its distribution overlaps with the location of OP at the time of sighting etc.


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Where do plants obtain the metal ions needed for biological processes?
Enzymes employ metal ions (e.g. Mg, Cr, Mn, Fe, Co, Ni, Cu, Zn) for catalysing certain reactions.
Let's consider planting a seed. Where will it obtain these metal ions from? Just from water?

Yes. From the soil.

@WYSIWYG then how hydroponics work? (Growth solution seems to only have N, P, K)

Even analytical ultra pure NaCl has so much Ca2+ in it that it would disrupt intracellular processes. Even if it says only N, P and K, there are still sufficient trace metal impurities.

@Ashafix ...which come from the water content..?

Water and nutrients like fertilizer.

Many ions are absorbed by the plants via the action of bacterias. Fe or B for example require chelating action from microbes. P and S need to be oxidised to enter the plant as well.
Source: Le sol, la Terre et les Champs - http://www.sangdelaterre.fr/index_135_151.html

The question is a little bit dubious, because when the OP says "seed" we tend to think about the seed before germination.
If you are talking strictly about the seed, it doesn't absorb from anywhere: the seed normally contains inside it all the macro and micro nutrients necessary for the first days after germination.
Of course, after a while, the growing sporophyte will need more macro and micro nutrients. These nutrients are already dissolved in soil (or in the water, for the aquatic plants), as non-charged compounds or as ions, and are absorbed mainly by the root system (whose cells have several different channels for absorbing them).
When the soil is poor in one of these nutrients, very interesting evolutive strategies may develop to obtain nutrients, as in the "carnivorous" plants. Note: the nutrients are classified in macro and micro not by the size or the weight of the atom, as the name may imply, but by the amount needed.

I'd like to add a small correction here. In plants the major micronutrient is glucose, which the  plant synthesizes from carbon dioxide and water (mainly)...so you should omit the word 'macro'-nutrients here.


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Lifetime of secondary messengers such as Calcium or IP3
Can anyone suggest me literature on the lifetime of secondary messengers such as calcium or IP3? A book would be preferred. What I am specifically looking for is a validation that secondary messengers have a certain lifetime and undergo degradation. I need not know specifically how long their lifetime is but rather interested in the fact that they do undergo biodegradation.
[EDIT]: Replaced the word 'biomolecule' by 'secondary messengers' as per the suggestion of @WYSIWYG to narrow down the answer.

The lifetime of Calcium can be considered infinite in biological time scales, it is not a real biomolecule. The half-life time of other biomolecules like IP3, PIP2, receptors, hormones, etc. is species-dependent and within the species strongly depending on the cell and its metabolic state.
Short answer: There is no overview for lifetimes of biomolecules. It is easier to search for a specific molecule in a specific cell. Perhaps you are lucky and somebody measured it.

Update to the comments:
All known second messengers, like Ca2+, IP3, PIP2, change their concentration in response to a stimulus, e.g. activation of muscarinic receptors causes activation of phospholipase C which cleaves PIP2 in DAG and IP3. IP3 causes release of Ca2+. Ca2+ never gets degraded or synthesized but the intracellular concentration changes. PIP2 gets degraded, i.e. its concentration becomes lower, while the concentration of its cleavage products, IP3 and DAG, increases. Those changes are temporary, after removal of the stimulus the 2nd messengers get degraded as well or e.g. Ca2+ is taken up into intracellular compartments.
A general overview about second messengers.

Thank for the info. But is there any book that talks about the lifetimes of biomolecules in general.

I doubt that there is a book in general. There are specific works, e.g. for IP3 and tables for drugs (can be found in most pharmacology books) but I don't recall any table for biomolecules in general. You might be lucky to find info on lipids or hormones in a review but it will require quite some work to compile a table for all biomolecules.

Not a single book that would say that biomolecules have a lifetime. I do not need to know how long the lifetimes are, but just a confirmation that any biomolecule would have a limited lifetime

I think the OP is referring to lifetime of Ca in active levels during a signalling event. Similarly with IP3 (related post). @nashynash clarify the question if that is the case.

If biomolecules would mean second messengers, then the question would be a lot easier to answer :)

@WYSIWYG  Like I stated, I want to know for the general case. I mentioned calcium and IP3 as an example. However, what you pointed out is true. But I still require the general case- lifetime of biomolecules. So I think my question stands correct to what I want.

@Ashafix what is the difference between a biomolecule as a secondary messenger and otherwise. Yes, like wysiwyg pointed out, more specific is about the secondary messenger type of molecules but I was hoping to find a general reference

A second messenger, like Ca2+ or IP3, is produced/released/degraded after a primary messenger, like a hormone, activates a receptor which is usually in the cell membrane. Biomolecules are all types of molecules produced by living organisms.

@nashynash Technically, Calcium can never perish. So your question does not make a lot of sense unless you narrow it down to a situation.

@WYSIWYG Okay. Thanks for the correction. Will narrow down the question.

@Ashafix okay. Thanks for providing the clarification and the update. However, besides the link you provided, can you suggest other sources from where you may or may not have referred to for the update?


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short-day facultative plant, abrupt change to photo period
What happens biologically to a short-day facultative plant that is a few weeks into its short day (flowering) photo period and is suddenly given a 24 hour period of light? Does anything change biologically after one day of long day (vegetative light) or  will it take several days?
If there is any biological change that is of concern what can one do to try and alleviate any negative affects?
https://en.wikipedia.org/wiki/Photoperiodism -

Please clarify - which plant are you speaking of, and are you saying it is already flowering - decided to answer anyway.

Yes in this example the plant is already a few weeks into flowering photo period. I am curios in regards to the entire class of short-day facultative plants.

There is nothing you can do to alleviate the effects of (presumably) gro lights being left on for a 24 hour period. It's not likely to have a particularly dramatic effect on a short day facultative plant, other than to possibly delay flowering - it may mean the plant has to go through an extra period of darkness at nights for a longer time, in other words, the process of flower induction may need to start all over again. Or, as it was just one night, you might get away with it and they'll flower when you expected them to. The biggest interruption in the flowering process of a short day plant is a few minutes light in the middle of a period of darkness over successive nights, but either way, it's not possible to offset that 24 hour period of light in any way. I'm afraid you'll just have to wait and see, but in the meantime, maintain the growing routine with regard to lighting.


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What is the exact percentage of spectral changes that human pinnae introduces into the acoustic input signal?
I read somewhere that amount of spectral changes that human auricula introduces into the input signal is 6%.
Now I cannot find that literature.
Does anyone know a source that might confirm this, or may confirm this him/her self? Well or contradict it if necessary.

%of what? dB per frequency band? It depends on various factors, including the acoustic frequency. Could you specify your question?

Even that is OK info. I am looking for any spectral change introduced by pinnae. Someone just put out, I guess a summarized percentage for all changes caused by pinnae. Intensity/freq ratios i.e. power spectral density changes are fine, if you know where to find the info.

I can have a look for a decent paper. Please give me 24h. Perhaps adapt your question accordingly as it is quite vague. It may help me and others to formulate an answer. And what do you mean with even that is OK? What is it that you want to know? Be specific. It's a cool topic though. Happy to spend my time on this :)


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What is the genetic difference between two cone branches?
As we can see on this larch, male and female cones are sometimes directed to grow on the opposite side of the branch. We were told in school that this mechanism works against self-fertilization. Also they flower in different times, so they are mostly fertilized from the other conifers.
When I saw this picture, I got that idea, that maybe they face the branches on above by design: To decrease the genetic uniformity at least a little.
But how important this effect actually is? And how big is the genetical difference between two branches? Are there any other factors taking effect in the tilt of the cones?

I don't understand your hypothesis. But the number of pairwise differences between two cells assuming neutrality ($\pi$) in the two different branches in $\pi = 2 \mu L t$, where $\mu$ is the somatic nucleotide mutation rate (around $10^{-11}$ on average), $L$ is the length of the sequence of interest (eventually the whole genome). $L$ can therefore be of the order of $10^9$. $t$ is the number of cell generation since the two cell lineages split. $t$ depends on the relative positions of the two branches but it could be $10^4$ cell generations. With these very quick approximations, we can estimate the number of pairwise differences as
$$\pi = 2 \mu L t \approx 2 \cdot 10^{-11} \cdot 10^9 \cdot 10^4 = 200$$

My hypothesis was it is a significantly better for the branch to be polynated from another branch than from the same branch, This number seems really huge if 2 is a significant genetic difference in Tajima's D, doesn't it? Question is, wheter this could play a role in the evolution of the branch structure.

This number should be verified with better estimates (typically the mitotic mutation rate might be way too high) should probably be compared to the number of pairwise differences in the population. The number of pairwise differences between two randomly sampled indivdiuals in the population is $2 N \mu$.

I am not sure why you are talking about Tajma's D. If I remember correctly (am too lazy to make the calculations now), Tajima's D compute a standardized comparison between the number of pairwise differences  number of segregating sites in a sample of size $k$ divided by $\sum_i^{k-1} \frac{1}{i}$ as both should equate under the infinite site model (coalescent theory).

Oh, sorry. But is it possible that this effect could play a role for example in the evolution of scape stem branching

Intuitively, I would think it is negligible but I am not sure.

Having separate male and female cones reduces self-fertilization just by the physical separation (the greater distance for pollen to travel gives pollen from a different tree a larger chance of successful fertilization).  A much larger effect is from the timing of flowering, since on an individual tree the female cones will be receptive at a time when the male cones on that tree are not releasing pollen.
Another reason for the different orientation of the cones is probably gravity.  The male cone, hanging downwards, can have its pollen fall out of the cone into the air where wind can transport it.  The female cone, pointing upwards, can capture settling pollen into its upward facing structures.


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Minimal viable EEG equipment for dissertation research on BCI / BMI
I am planning out a dissertation study of Brain-computer Interface (a.k.a. Brain-machine Interface, BCI, BMI, etc) applications.
One of the 3 papers in that dissertation will involve collecting original data, analyzing it, and writing a biofeedback application based upon this data.
I'm in a Computer Science department at a university which does not have a med school, so as far as I know I'll have to purchase the equipment myself out of a very modest research budget.
Thus, my question is "what's the lowest-end (i.e. cheapest) kind of EEG machine which would still be considered modern and sophisticated enough to be publication worthy in journals?".
Of course, I've done a good bit of research on this by reading recently publications on Google Scholar and will continue to do more research, but there's a lot of information overload and I have no prior background with EEG equipment, so any insight would be greatly appreciated.
From what I can tell the main thing driving price is the number of leads or sensors. They seem to range from 1 lead in consumer EEG toys to 100 leads, with a lot of products being advertised that have 16 or 24 leads. There are of course a lot of other features, so feel free to answer using either specific products or in terms of whatever features you've found important.

I have been working with BCI since some time and would recommend you to try these ones. They all have been widely used in MS/PhD research and their results are more or less accepted everywhere:

Emotiv
NeuroSky  (Starts from 99$)
g.tec (Most accurate/Expensive one - not recommended for startups)

P.S: Last, but not least, feel free to have a look at BCI Competition datasets. I remember I used them in my semester project. Plus, if you are interested in getting the dataset of invasive BCI, I can provide you the email of respective research as well. Best of luck in your Research!!

That's highly useful! Neurosky only has 1 sensor though, right? Is that enough for most purposes?

@Hack-R I would recommend you Emotiv (hence first in list). Emotiv has been used by MS Thesis students regularly here, so its quality would do for you!


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Resting stage of primary oocytes
In my biology textbook, I read that the primary oocyte gets arrested in the early stages of meiosis in prophase I (diplotene stage). I wanted to know why this is so. I searched google, and this phenomenon is known as dictyate. Furthermore the source was talking about translational arrest after transcription. Why does it occur during cell division? Moreover, what's so necessary about this phenomenon?

Could you provide a link to the article from your google search?

http://www.embryology.ch/anglais/cgametogen/oogenese01.html

I am not sure if I can answer the question of why the primary oocyte gets arrested during meiosis (and finishes after fertilization), but the stage of growth the egg is arrested at does vary widely between species; it's not always primary oocyte. This might suggest that the reason is species-dependent.

In sea urchins, it's the fully mature ovum that gets fertilized.
In humans, it's the secondary oocyte (arrested during this stage of meiosis) that gets fertilized.
In the majority of mammals (dogs, etc.), it's the primary oocyte that gets fertilized. In both of these last two, the oocyte finishes meiosis after fertilization & the entry of the sperm nucleus into the egg.

The translational arrest of the egg you mentioned is because the egg is in a "dormant" state until it is fertilized, and it is "activated" by fertilization. Until fertilization, the mRNA's are present in the cytoplasm, but cannot be translated because they are missing poly-A tails (translational arrest); free levels of calcium in the cytoplasm are low; and respiration and oxygen levels are low. This is because the egg is "primed" for the explosion of activity necessary during early development (taking place after fertilization); the mRNA's code for proteins that are used at that time, but they are not translated until fertilization.
Source: http://www.ncbi.nlm.nih.gov/books/NBK10029/ (see the second paragraph under "Late Responses")


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How is a T lymphocyte specific to an antigen but not specific to an epitope?
In my immunology notes, it states that B lymphocytes (and other APCs) capture and present antigens to T lymphocytes that is specific for an antigen, but that the T cells do not necessarily recognise the same epitope. How can a cell be specific to an antigen but not to the epitope presenting on the surface of the antigen?
I've been in the process of discussing this with a friend and trying to make sense of Janeway's immunobiology and we've come to the theory that the APC recognises the antigen and takes it up, breaks it down and presents the epitope via the MHC where it is then recognised by the T cell. Am I right in saying that the antigen is broken down into many fragments that act as epitopes but each clonal expansion of T cells can only recognise the various epitopes of one antigen?

It's mainly because antigens have multiple epitopes, and so the T/B cells will recognize one epitope, but you'll get multiple cells recognizing multiple epitopes. The polyclonal expansion of these cells allow the attack to come at multiple angles of the same antigen at once.

Okay, I think I understand why T/B cells can bind multiple epitopes but I'm still confused about how this leads to them being specific to one antigen, as surely, different antigens could have the same epitopes on them? Or is each type of epitope only found on one antigen? Thanks for your help! @CMosychuk

Take a look at the following image. The shapes on the bacteriums surface are the antigenic determinants, aka the epitopes. Notice how they can differ: each antigen has many epitopes at once.

Thanks for the image, it really helps me to visualise it. I think my confusion is coming from the fact that on my midterm (will edit the post and tag homework, I read the rules after posting) it says that "Concerning T lymphocyte/B lymphocyte co-operation in humoral immune responses to T dependent antigens:
The epitope recognised by the T cells and B cells must be identical (FALSE)
The antigen recognised by the T cells and B cells must be identical.  (TRUE)"
And it's the second statement that's confusing me. I don't understand that bit, does that make sense? @CMosychuk

"...it states that B lymphocytes (and other APCs) capture and present antigens to T lymphocytes that is specific for an antigen" - Shouldn't it read"...present epitopes to T lymphocytes..." or "...present peptides" (that's what they are? Which leads to: Do presented peptides have/include epitopes, or: embed one and only one epitope). -  Ref. @CMosychuk – Elizabeth May 30 '16: Do you mean:  if B-Cells "edit" one and the same antibody they are specific for, they are being "activated" from different sides (even different strains of virus causing that activation)?

For this answer lets restrict ourselves to T dependent MHC II mediated responses.
So, an APC like a macrophage or a dendritic cell, takes in a pathogen by phagocytosis and degrades it inside the cell. Some of its broken proteins, which are antigens are presented on the MHC II of this particular APC.
The B cells also do something similar but they identify either free floating antigens or the ones that are expressed by phagocytic APCs. These antigens are broken down in the lysosome. These fragments now are expressed on the surface along with MHC II. This fragment may or may not contain the epitope that the B cell receptor (surface antibody) originally recognised the antigen with. Also, it is not that just one of the fragment is taken to the surface, most of them make it, each with a separate MHC.
The T cell that is going to now interact with this B cell may have a TCR (T cell Receptor) against the epitope in any one of those fragmented antigens on the MHC.
This T-cell is specific to that particular epitope of the antigen it bound to, similarly there could be another T-cell that could recognise some other fragment of the same antigen brought to the membrane by a different MHC II.
So, the epitope that the B-cell and the T-cell recognised the antigen with, needn't be the same. But logically, there's a possibility that they may be.

Note that:

The processing of antigen in the phagocytic APC is not shown in the picture.
B cell recognises antigens not that are displayed on the MHC II (this the T cell does) but those that are tethered on the APC membrane.

Image: Nature Reviews Immunology.

"The B cells (...) identify either free floating antigens or the ones that are expressed by phagocytic APCs." - 1. True that B cells do not take up whole viruses? 2. Any basic textbook reference for APC presenting, then B taking up? 3. Still true that cytotoxic T cells do not uptake, in contrast to B cells(!)?

Perhaps it would simplify for you to think of a model system? Let's take HIV because it's simple. The antigen in this case is a protein called ENV and it looks like this.

All of those arrows are pointing "regions" of the antigen that an antibody will bind to. Since the B cell makes the antibody you can think of these regions as where the B cell will bind to. They call these regions epitopes.
Do you see how there are many different sites on one antigen? Well one of those epitopes can be for a B cell and one of those epitopes, which can even be on the other side of the antigen, can be an eptiope for a T cell. So while T and B cells recognize the same antigen, in this case HIV Env, they needn't bind the same epitopes.

I think where you may be getting confused is  when B cells chew up an antigen, the epitope they display on MHCII and display to T cells is not necessarily the same epitope it used to recognize the antigen. The B cell chews up the entire antigen, including T cell epitopes, and displays them on MHCII.

I think it's worth mentioning in that context that B cells only produce antibodies that refer to the epitope they recognize, not the ones they present to T helper cells (as I feel rather insecure about that...).


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What drives male fish to spray their milt?
In mammals the sexdrive of the males is because the intercourse provides a satisfaction where after, the sperm is ejaculated into the female. However, the male sperm doesn't enter the female fish but reproduces by spraying this fluid which contains the sperm, onto roe (fish eggs).
But what kind of (physical) drift is urging them to spray, while they probably don't have an orgasm, or do they?

From a human perspective, it's easy to understand how feelings of sexual attraction and an urge to have sex result in people reproducing. For men, this may be most apparent in the extreme pleasure found at the moment of orgasm, which coincides with insemination. However, there are many behaviors that people have a tendency to perform that don't involve any sort of immediate pleasure comparable to an orgasm.  For example, if someone cuts their finger, often their initial instinct is to stick their finger in their mouth. This is a type of wound licking, which is observed in a number of different species of mammals and is believed to promote wound healing due to clotting factors, growth factors, and/or antimicrobial factors present in saliva. However, a young child who cuts his finger sticks it in his mouth without any knowledge of these biological processes. It's a behavior that we are genetically programmed to perform because it promotes healing and reduces the risk of infection, thus promoting survival, thus promoting eventual reproduction. It has therefore been favored by natural selection.
There are many behaviors in animals that are clearly genetically programmed, and which animals perform consistently given the right stimuli (i.e., the right "triggers," whether they be visual or via other senses). Here are a few examples off the top of my head:
In birds, the process of mating and raising young is long, complex, and laborious. The process begins well before and continues well beyond the actual act of copulation (when insemination occurs). This suggests that there is some sort of more general internal mechanism that motivates the birds to go through these costly, time-consuming, stereotypic behaviors, generation after generation, in order to reproduce.
As a quick overview of some of these reproductive behaviors:
Many birds go through the effort of migrating long distances to very specific locations that they use as their breeding grounds and/or nesting grounds. The travel alone is energy-intensive and can be dangerous or even fatal. Mating is often preceded by complex courtship behaviors, sometimes involving elaborate song-and-dance performances by the males (video), in an attempt to impress the typically picky females. In some species, such as manakins, juvenile males may practice their courtship performance (video) for several years before using it to actually find a mate, as the execution needs to be flawless in order to sufficiently impress a potential mate. The young males use their male peers as stand-ins for the female during these practice sessions or rehearsals.
If the female is satisfied with a male suitor, then they may pair up and create a nest. The parent birds build their nests in very exacting and particular ways, even though they themselves don't even live in a nest the rest of the time. It's constructed purely for the purpose of raising chicks, and is abandoned after the chicks leave the nest. Yet the parents have some desire or "push" to build it, and to do so in very precise and structurally sound ways (in terms of climate, location, distance from the ground, materials used, size, shape, etc.). Eggs are laid, and when they hatch, a great deal of effort goes toward feeding the hungry chicks with their gaping mouths and helpless cries for more food, day in and day out, often for several weeks or months. I doubt that the motivation of either the mother or father bird is comparable to the human experience of sexual pleasure, so there is something else that prompts them to go through this ordeal, year after year.
Would we say the parent birds experience intense pleasure that motivates them to do all of this, in the right order, at the right time, and with such precision? It's impossible to know what a bird is "thinking," but remember that there is a danger in trying to project human emotions onto animals, whose brains may function in ways rather different from our own.
Interestingly, the sight of a young bird's open mouth is apparently a strong trigger for the parent bird to "want" to put food in that mouth. Evidence of this includes the fact that some bird species don't build their own nests or raise their own young at all, but rather lay their eggs in other birds' nests (quickly and sneakily, while the parents are away). The parent birds residing at the nest (i.e., the hosts) often don't notice the difference between their real offspring and the intruder that's a different species (i.e., the parasite), even though the difference is often obvious to any human observer. As a result, the the unwitting host parents feed and raise the parasite bird as if it were their own, often to the detriment of their actual chicks. The parasite chick species is often larger and grows faster than the host species, so the parasite outcompetes its host siblings for food (and sometimes pecks them to death or pushes them out of the nest). The parasite often grows much larger than its parents, yet the parents continue to expend lots of energy feeding it, as if they are unable to override whatever program that normally guides their behavior, because the sight of the parasite chick's open mouth is such a strong trigger.

Even stranger, perhaps, is the fact that multiple different species of birds have been observed feeding fish (often koi/goldfish in ornamental ponds or parks) as if the fish were their own offspring. The fish swim to the water's surface and open their mouths, and the sight of this drives certain birds to go find food and bring it back to feed to the fish. According to one source (in the following video), the feedings occurred up to six times per day.  Here's that video: A cardinal feeding several hungry goldfish.
Enough about birds, though; let's talk about bees.  Actually, not bees, but their close relatives, wasps. Among wasps, parasitoid wasps are a large group estimated to contain over 600,000 different species worldwide. An example that you may have heard of is the tarantula hawk wasp, which attacks, stings, and paralyzes (but does not kill) a tarantula "victim," then drags the tarantula to a prepared burrow/nest location, lays an egg on the tarantula's body, seals off the nest with the paralyzed (but still living) tarantula and wasp egg inside, and then flies off, never to see the offspring again. When the wasp egg hatches, the wasp larva bores a hole into the spider's abdomen, eating the living spider's insides while carefully avoiding the vital organs for as long as possible. This keeps the spider alive as it gets eaten from the inside out, and thus prevents the larva's food from rotting. Interestingly, as adults, these wasps subsist on nectar and plant material. The males don't hunt prey at all, and the females go through the process of attacking tarantulas (which are much larger than themselves) just so that they can drag the spider to the prepared burrow for their offspring to eat later. They don't even witness the fruits of their labor — but they are motivated to go through this process nonetheless.
While the process would seem to require some skill and intelligence on the part of the mother wasp, in some ways it seems overly pre-programmed and inflexible.  For example, consider the following description of the behavior of the parasitoid wasp genus Sphex, relayed by D. E. Wooldridge in The machinery of the brain in 1963:

When the time comes for egg laying, the wasp Sphex builds a burrow
for the purpose and seeks a cricket which she stings in such a way as
to paralyze but not kill it. She drags the cricket into the burrow,
lays her eggs alongside, closes the burrow, then flies away, never to
return. In due course, the eggs hatch and the wasp grubs feed off the
paralyzed cricket, which has not decayed, having been kept in the wasp
equivalent of a deepfreeze. To the human mind, such an elaborately
organized and seemingly purposeful routine conveys a convincing flavor
of logic and thoughtfulness — until more details are examined. For
example, the wasp’s routine is to bring the paralyzed cricket to the
burrow, leave it on the threshold, go inside to see that all is well,
emerge, and then drag the cricket in. If, while the wasp is inside
making her preliminary inspection, the cricket is moved a few inches
away, the wasp, on emerging from the burrow, will bring the cricket
back to the threshold, but not inside, and will then repeat the
preparatory procedure of entering the burrow to see that everything is
all right. If again the cricket is removed a few inches while the wasp
is inside, once again the wasp will move the cricket up to the
threshold and re-enter the burrow for a final check. The wasp never
thinks of pulling the cricket straight in. On one occasion this
procedure was repeated forty times, always with the same result.

On a similar note: Normally, the female wasp grabs the paralyzed cricket by its antenna to drag it into the burrow. However, if both antennae are cut off while the wasp is briefly away, then she is unable to pull the cricket inside and complete her task. She doesn't even attempt an alternative, such as pulling it by one of its legs, even though that would seem like an obvious backup plan to the human mind.
So, what motivates the female wasp to go through all this trouble in this way?  Is this even an example of true "motivation," or is it simply a form of genetic determinism in which she is an automaton, unable to modify her actions? It's food for thought.

Although this comment was very well written regarding animal motivations in general and how we should be careful with ascribing human emotions to animals, I think you forgot to relate it back to the original question, which was specifically about fish.

@ETam If someone asked what causes an apple to fall downward from a tree, the most meaningful response would not consist primarily of a lesson in botany or horticulture. In order to understand why an apple falls downward from a tree, one ultimately needs to have some understanding of gravitation as a general physical phenomenon. Whether the mass being acted upon by gravity is an apple, a boulder, or a planet, the underlying explanation is the same, and it has little to do with apples, boulders, or planets, specifically. Likewise, this question, ultimately, is not about fish.

Assessing the motivation of gamete release in fishes is difficult, but most if not all organisms have a drive to reproduce, which likely instills some feeling of satisfaction if the species is capable of such feelings. From numerous observations of fish spawning, I am not sure that I would use the word spray for the release of milt. Such fishes are only capability of external fertilization, where females either deposit eggs or release them into the water column. Males will release milt either over deposited eggs or pelagically at the same time of egg release. The observed spraying is caused by the release of milt into a fluid that disperses and mixes it in the water column with eggs for fertilization. Water movement coupled with the movement of the male fish results in the perceived "spraying." The functionality of this type of dispersal is to mix the sperm with eggs, both of which are subjected to fluid dispersal. Numerous videos show this behavior in Rowell et al. 2018 supporting info videos https://onlinelibrary.wiley.com/doi/10.1111/jfb.13888 There are numerous other videos out there as well.


text:
How does an increase in CO2 concentration affect Photosynthesis and Transpiration
I noticed a strange thing in my book. At one place it says that an increase in CO$_2$ concentration in the outside air decreases the rate of transpiration but at the other place it says that an increase in the level of CO$_2$ in the environment increases the rate of photosynthesis?
Can we reconcile between these two statements? I don't think so because both the processes mostly take place through the stoma so how is it possible that when transpiration decreases photosynthesis increases ?How ?

great! could you please also link to the literature you are referring to?

@JordiZambrino i didn't get you ..... what do you mean by the literature i am using?

By literature I mean what book you are reading.

@JordiZambrino. .. i m using ICSE Concise Biology


text:
How to retrieve logical expression (KO based) for reactions from KEGG?
Whether a module is complete or not can easily be checked by evaluating the Definition entry associated with the module; e.g. in module M00010, it is given by
Definition  K01647 (K01681,K01682) (K00031,K00030)

which can be translated to
K01647 AND (K01681 OR K01682) AND (K00031 OR K00030)

If this expression evaluates to TRUE, the module is complete.
Now I am wondering whether analogue information exists for a single reaction. So e.g. for R00352, one finds the following information about Orthology:

But how do I now know in which logical relation the KOs are?
So it could be
K01648 AND K15230 AND K15231

or
K01648 OR (K15230 AND K15231)

and so on.
Can this information be retrieved from KEGG and if so, how?
EDIT:
In the above example, the correct expression would be:
K01648 OR (K15230 AND K15231)

One either needs K01648 or the other two subunits together. So, unfortunately, it is not as easy as @aretaon describes it in his answer since just one of the two subunits would not be sufficient. One can therefore not just connect the KOs associated to a reaction using a logical OR.

To rephrase what you already mentioned in your question: For a KEGG Module to be completed (so that an organism can perform a certain function) you need a certain set of functional units or enzymes. So to evaluate the abilities of an organism you would check its genome for the gene sequences related to the module by performing the logical operation you mentioned above.
A Module is composed of chemicals (C) and reactions (R), as you can see in your given example. To explain the differences between modules and reactions best have a look at the last reaction, Isocitrate to 2-Oxoglutarate. There are three boxed reactions (one of them is a combination of two) that all lead to Oxoglutarate. When you look at the Orthology (the enzymes involved) for the reactions in the first box (R01899+R00268) and the second box (R00267) you will see, that it's the same enzyme (K0030) performing different reactions. The third box now contains a reaction (R00709) performed by a second enzyme (K0031), that leads the same way (it differs in using NAD+ instead of NADP+ as electron acceptor). So for the module to be completed you could use either of the two (that’s the reason for the OR-operator in the logical operation).
If you now want to evaluate if a certain type of reaction occurs in a given organism it is sufficient to have one of the possible enzymes catalysing this reaction. So:
K01648 OR K15230 OR K15231

Thanks for your reply. Unfortunately, it is not that simple (see my EDIT), but I wish it was... ;)

I tried to find another way but I think there is none. The logical syntax you describe is defined only for modules - and modules cover only selected parts of all pathways. So to be certain if the enzyme in a reaction is only part of a multi-enzyme complex (as in your example) you even cannot go back to pathways because the required parts aren't defined there either.

Yes. I tried to infer it from the module structure and the reaction list but that doesn't work either since that is inconsistent between modules, unfortunately... Too bad that there is no solution to this issue, it seems.


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Without plant breeding and domestication, would most of the foods consumed by humans evolve to become inedible?
Would this happen? Do species evolve to avoid being consumed, especially the animal species which have no need to leave seeds?

Plant defense against herbivory
Plenty of plant species evolved defense mechanisms. There is a large variety of defense mechanism. Have a look at the wikipedia article Plant defense against herbivory for more information. Such defense mechanism often comes at a cost and therefore the mechanism can be maintained only if herbivory is sufficiently common and costly. Note that herbivory might be beneficial to some animal species typically as it can help to disperse the seeds.
plant-herbivores Co-evolution
Herbivores co-evolve with plants and develop mechanism to deal with plant defense mechanism. Such coevolution often yield herbivores to specialize in feeding in a handful of plant species only.
Human consumption
Most of what human consume is artificially selection. We specifically allow the breeding of individuals that present trait that are pleasant to us. In such condition, a defense mechanism would be a highly deleterious trait.

Do species evolve to avoid being consumed, especially the animal species which have no need to leave seeds?

I don't understand this sentence. Do you mean "[..] especially plant species being consumed by animal species that don't help spreading the seeds"?
If this is what you meant, then yes. If herbivory comes at non benefit for the plant, the overall cost of herbivory will be more important for the plant. All else being equal, a mutant that present a defense mechanism would have a higher fitness if the herbivores do not offer any benefit to the plant being eaten.

It's a yes or no question

If you rephrased the question "without artificial selection" instead of "without breeding and domestication" (which sounds really alike but has the advantage to clarify your question), then the answer to the title question (there are actually more than one question in the post) is yes if we assume that our consumption comes at a cost (that outweigh potential benefit) to the plant and note that it may take quite a bit of time for it to evolve.


text:
Is cell wall and cytoplasm an organelle?
So cell wall is an organelle?
Whereas, it is not a membrane-closed organelle?
Cytoplasm is an organelle?
Whereas, it is not a membrane-closed organelle?

For me it looks much like a matter of just terminology and definition. Cytoplasm is a part of cell so I could not see any cause to deny cytoplasm as an organelle. Is that?

From viewpoint of definition I couldnot tell the cell wall as 'cell organelle' because it is out of the cell. In another term it is 'extracellular matrix'

Traditionally we call chloroplasts and mitochondria as organelles. But now it is well established that they are entire cells (including cytoplasm) of other species! however still we call them organelle.

@AlwaysConfused This is a semantic question without any real value in biology. I'm going to vote to close since this ultimately comes down to a matter of opinion without more information or a detailed scientific question. i.e cell biologists may care about the organization of all sub-cellular components, so the cytoplasm is important, whereas biophysicists may count it as exceptional since luminal spaces are more akin to extra-cellular spaces than the cytoplasm, so it's a very different cellular structure to them.

The cell wall isn't an organelle (according to VCE biology textbook) and the cytoplasm is not.
My guess is that the wall regulates movement (ie, active function), whereas cytoplasm is just a fluid in which the other cells are surrounded (ie, passive).
http://www.edu.pe.ca/gray/class_pages/rcfleming/cells/notes.htm
Note that the terms active and passive are not being used in any scientific term, but are rather referring to if the mentioned item is actively carrying out (a) process(es)

Please add some reference(s)!

Cytoplasm is not reduced to cytosol!

I was not saying it was. It is water, salts and proteins.

How cell-wall could be a cell-organelle? it is extracellular matrix (out of cell)

whereas cytoplasm is just a fluid in which the other cells are surrounded (ie, passive). Just a passive fluid, is it? It's the bedrock of all life as we know it! "Passive" indeed... :P

Wikipedia gives quite clear and sourced answers in this case:

an organelle is a specialized subunit within a cell that has a specific function. Individual organelles are usually separately enclosed within their own lipid bilayers.
Under the more restricted definition of membrane-bound structures,
some parts of the cell do not qualify as organelles. Nevertheless, the
use of organelle to refer to non-membrane bound structures such as
ribosomes is common.[11] This has led some texts to delineate between
membrane-bound and non-membrane bound organelles.[12] The non-membrane
bound organelles, also called large biomolecular complexes, are large
assemblies of macromolecules that carry out particular and specialized
functions, but they lack membrane boundaries.

To answer our question, the cell wall can be considered an organelle as it is a subunit with a defined (set of related) function(s).
The cytoplasm in itself is difficult to consider as an organelle, but the cytoskeleton can be considered one.

Cytoplasm is not an organelle. This is simply a generic term that describes everything within the plasma membrane and outside the nucleus.
We typically think of organelles as being within cells. The cell wall surrounds the cell, lying just outside the plasma membrane, usually considered the boundry of a cell. On the other hand it provides vital function for the cells having them and could be considered an organelle in this context. While it offers some regulation of passage of substance between cells, its principal function is support. I would have accepted either yes or no from my high school students.
(I'm about to depart to a 6th grade class to lead them in an activity demonstrating the support function of cell walls! Balloons. i.e. cells, inside heavy paper bags, i.e. cell walls.)


text:
Microscopy of moving white blood cells
Is there a way to get white blood cells to move while on a microscope slide? I want to try to get some microscope images of them moving, but so far I have only found them stationary.

Not an experimentalist, so take this with a grain of salt.  But for motility you often need some external factor, e.g. a chemokine or chemoattractant (FMLP is a common one for white blood cells).  Also some cell types may not crawl on bare glass, and might need a protein or gelatin coating.
White blood cells on slides can look like this: https://www.youtube.com/watch?v=JnlULOjUhSQ
Unfortunately, I don't know the conditions used there.  My recommendation is to look through Google Scholar for white blood cell motility or neutrophil motility, and see what turns up.  For instance, the first paper I found was: C S Spada, A L Nieves, A H Krauss and D F Woodward, J. Leuk. Biol. 1994 (PDF) which gives some details about how they got their assays to work, including a gelatin coating for the slides.  However, the details probably depend on the origin of your cells and the type of white blood cell you're looking at.

White blood cells move. As long as they're alive, they move, but they do it veeeeeery slowly.
The movements can be seen using time-lapse photography.
See: https://www.wetenschapsforum.nl/index.php/topic/199938-levend-bloed-onder-de-microscoop/
These were made at about 1,000x, anoptral contrast.


text:
How do cancers eventually lead to death / other debilitating symptoms?
With regards to people I know or have read about who live with cancer, most of their symptoms are results of chemotherapy, surgical interventions, etc., which have the goal of eradicating the cancer. Assuming the cancer went untreated,* what kinds of symptoms would the cancer itself lead to, and by what mechanism would it cause death (in most cases)?
Please excuse my ignorance. I know that every cancer is different, and even different cases of a single type of cancer can present differently; so there may be many different answers to this question, but I'm not sure if they eventually lead to the same thing.
*I'm asking purely out of curiosity – I'm not "opposed" to chemotherapy or anything like that.

Where did you read about what symptoms? And I can assure you, cancers alone have a lot of nasty syndroms and outcomes.

Thank you for the comment--I would believe that for sure, I'm just wondering how specifically the cancer will kill / lead to the nasty symptoms. I'm mostly thinking about a personal case, where someone suffering from AML went through many rounds of chemo and developed a bad infection as a result of immunosuppressants. We didn't hear about symptoms of the cancer simply because the doctors detected it early and (thankfully) didn't let it get to that point.The book I'm reading is "The Emperor of All Maladies" by Siddhartha Mukherjee, which admittedly focuses on the history of cancer treatments.

This is a very general answer to a very general question.
So, in general, cancer occurs when cells stop behaving as they are supposed to.
Your body is made by something like 200 different kinds of cells (epithelial cells, neuronal cells, blood cells and so on) working together to maintain the body's functions. If many of those cells stop doing what they are supposed to do then your body will start malfunctioning. Different kinds of malfunctioning will occur depending on what kind and on how many cancer cells will spread throughout your body. This can eventually cause system failures.
If your lung cells are malfunctioning, for example, you may expect respiration problems.
Often cancerous cells spread all around your body (metastasis) and several tissues and organs will be compromised simultaneously leading to a complex pattern of symptoms.
Fatigue, pain, inflammations, and bleeding are common symptoms in many advanced stages of cancer since tissues and organs start to get seriously damaged.

Thanks for the answer--this explains what I was wondering about. Is it possible for a cancer to interfere relatively small amounts of interference with the function of healthy tissues? For example, with lung cancer, if the other lung would continue to function, or what remains of the healthy tissue of the cancerous lung. In these cases, would it be metastasis that leads to inhibition of vital healthy tissues around the body? Thank you again

Yes, small cancers can pass by unnoticed for a long time, they do not affect the overall function of the tissue or organ. It depends on how spread the cancer is. Indeed, in many cases, people start feeling sick after the cancer is already spread and so the doctors diagnose it when is unfortunately too late to remove it with a simple surgical operation. The problem is that sooner or later cancer will spread, so to eliminate the source of cancerous cells asap is important.


text:
Living on pure glycogen?
I was recently fascinated when I learned about polysaccharides (I am a biology newbie) and was wondering about some of their properties. After doing some googling I was unable to find any information regarding this scenario.
This is purely theoretical, I am not insane enough to actually try this.

If my only source of carbohydrates was ingestion of pure glycogen,
could I live healthily? (assuming I obtain all other necessities for
life)
Approximately how many grams of glycogen would I need to live for a
week (assuming I weigh 150 lbs)? Is this even possible to calculate?
What does pure glycogen taste like?

See http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802397/ yes if you take glycogen alongwith proteins, fats, etc. you can survive. As for taste, I don't know how it tastes, it should be tasteless but should become sweet after some time due to action of enzymes.

If you added that as an answer, I would upvote it. It doesn't address question #2, but it is vastly better than the current lack of answers.

You asked three questions here, so I'll answer them one by one.

Yes, you can survive with glycogen as the only source of carbohydrates, assuming that you also take other nutrients like proteins, fats, vitamins, etc. also because carbohydrates cannot supplement all of them. See this article:

There are three macronutrients: carbohydrates, protein and fats. Macronutrients are essential for proper body functioning, and the body requires large amounts of them. All macronutrients must be obtained through diet; the body cannot produce macronutrients on its own.

No, there's no way to calculate this. If we were talking about glucose, a definite range could be given. But since glycogen is a polymer with variable amount of glucose molecules linked together (at least I couldn't find an exact number),  its not possible to tell how many glycogen molecules are needed for the daily metabolism in the body.

Glycogen is an organic, non-polar polymer, insoluble in water just like starch. It does not have a specific taste, but once you eat it, an enzyme called salivary amylase will break it into glucose, maltose and limit dextrins, causing it to taste a bit sweet. See this article:

This enzyme acts on starch, glycogen and related polysaccharides and oligosaccharides producing beta-maltose by an inversion.

Source


text:
Why does my eyes see a red spot when over exposed to light?
When I looked into my projector when it was on the blue screen it left a red spot in my vision. I should not have tried it but all the colors left a red spot. Why not a blue or yellow spot was left?

Did looking at a bright red light also leave a red after-image? Usually if you expose your eyes to a color, the eye becomes less sensitive to that color, and then shortly thereafter things will look more like the inverse of that color. If we're talking long-term damage, maybe it has something to do with the inside of the eye being red.

Without more details this is nothing more than an anecdotal report and your perception may have had nothing to do with that beamer in the first place. Personally, I would close this Q on the basis of that, but since your Q has received so many upvotes apparently it is appreciated by others.

You are describing the phenomenon of negative afterimages, a type of physiological afterimage, which is a result of how the cells in the retina work. Specifically, it is a result of the adaptation of photoreceptors.

According to the opponent process theory of color vision, our
  perception of color is controlled by two opposing systems: a
  magenta-green system and a blue-yellow system. For example, the color
  red serves as an antagonistic to the color green so that when you
  stare too long at a magenta image you will then see a green
  afterimage. The magenta color fatigues the magenta photoreceptors so
  that they produce a weaker signal. Since magenta's opposing color is
  green, we then interpret the afterimage as green.

There is a well-known illusion, called the negative photo illusion, which exploits exactly that. It is required not to move the eyes, because you need to bleach the photoreceptors in an exact place on your retina. This is why you have to fixate on a dot in the middle of a picture, otherwise the bleaching will not occur.
EDIT: I mention a two-axis (magenta-green system, blue-yellow) system, but the exact color system - which would predict which afterimage you would see - is most likely a trichromatic system, which includes red, green and blue channels, based on the principle of the three types of retinal cone cells. It is important to remember that this is a phenomenon in perception, and thus may, in some cases, not be reducible to the fact that there are three types of cone cells, or that bleaching of a photoreceptor has occurred. Please see the comment thread below for some clarification.

So OP should've seen a yellow afterimage. They, reportedly, didn't.

Of course you don't need to. I provided a detailed explanation as a comment under your answer. Would you prefer me to remove my downvote just to earn bounty points? That wouldn't be right in the spirit of science. @AliceD If the blue bleaching light was lighter, slightly green or cyan, it's opponent color would be red, as observed. See this illumination circle for reference

Of course a green light would have a red afterimage, but that's not what the question says.

Hi there. I'm sorry if I incorrectly interpret your comments as smug or highly pedantic. I'm not sure why such unnecessary and spiteful comments are being left, especially by a mod. The question states, why a red afterimage? to which my response, which happens to be scientifically accurate and concise, was because of cyan photobleaching and the opponent color phenomenon in visual perception. The question Why not blue or yellow? is well addressed. Demystifyingly, the questioner stared directly at a projector lamp giving off a light blue hue of light, which is common with projectors.

No need to feel offended. I do not support the answer, as the opponent system has two axes, namely a blue-yellow and a red-green axis. The answer suggests the existence of a blue-red axis. That's not conform the Herring Theory of opponent vision.

That's clear then. The phenomenon really seems to be based on an opponent color phenomenon. Whether it is the Herring two-axis theory, or a trichromatic one (the Young–Helmholtz theory, which better captures the triadic nature of retinal cone cells) is a more detailed discussion, I'm sure you'll agree. I would explain it simply though: if you bleach blue/green photoreceptors in the fovea, the negative image is based on the immediate and relative hyperactivity of red cone cells. It's possible OP confused red for orange in the afterimage, which would be the opponent color of blue. Cheers!

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