text:
What is the difference between effective and efficient selection?
I always thought of the efficiency of natural selection in the context of molecular evolution. I.e. that linked selection and smaller population size cause less efficient selection. It took me a while before I even noticed that people also say the efficacy of selection.
When researching the answer myself, I found that older papers talk more often about efficacy (like this one). I also found that besides the natural-selection context, it seems efficiency of selection is also used in the context of breeding (like here). However, you can certainly find cases when used in the context of natural selection. Finally, there are about 4x more papers that contain the words "efficiency" and "natural selection" compared to "efficacy" and "natural selection".
So, is effective and efficient natural selection the same thing? Is "efficacy of selection" and "efficiency of selection" be used interchangeably?
-- EDIT --
I am interested in the use of these two words in the context of natural selection only. Unlike in other contexts, in natural selection dictionary definitions of the two words do not make much sense.

I think it is a case of Humpty Dumpty in Alice in Wonderland. The words meant exactly what the authors chose them to mean, which unfortunately we cannot tell, because there is no authority that gives these English words precise definitions in biology. As I keep saying, biology is not physics.

I think that in this case, they are used synonymously, even though they do indeed have a subtle difference in definition. This is a common synonymy in biology, many researchers are not native speakers and there exist many native speakers who do not appreciate the difference between the two enough to use it with precision. For instance, here you see it used more or less interchangeably. Effectiveness, efficacy, efficiency...

@SPr Thanks, that's already a nearly complete answer. Would you mind also elaborating a bit about the subtle difference in this context? (also if you post it as an answer, I would be happy to accept it)

As a reader, when I read effective selection, it means it works, and is successful to a high degree. For example, 70% ethanol is effective at sterilizing your work bench (negative selection). It does the job well when you wipe several times with it. Conversely, when I read efficient selection, I read it as selection that is accomplished with the least amount of wasted time or effort. Paraformaldehyde or gamma ray radiation are more more efficient at sterilization (they work more stringently and the performance is better), but they are obviously not as practicable. Unsafe and costly.

The distinction made by @bob1 makes perfect sense:

Effective selection applies to the situation where selection may or may not work: e.g., in a small population subject to the random drift, the selection may be ineffective in the sense that deleterious alleles may fix with nearly the same probability as beneficial ones, the outcome thus nearly independent on the selection. On the other hand, in a sufficiently large population the outcome is largely determined by selection, i.e., the selection is efficient, as suggested in the first reference given in the OP:

Deleterious alleles can reach high frequency in small populations because of random fluctuations in allele frequency. This may lead, over time, to reduced average fitness. In this sense, selection is more “effective” in larger populations.

Efficient selection refers to the cost of the selection, as suggested by the second OP reference:

A new index of selection efficiency, i.e. the ratio of the probability of achieving the desired genetic gain in a target population to the cost expended for that gain, is introduced to define the optimum selection procedures that give the most opportunities for producing new commercial varieties.

The cost here may mean very different things - the actual financial cost to the breeder, the energy expenditure by organisms, the number of generations necessary for achieving the desired outcome. Thus, selection may be effective in the sense that we do arrive at the desired resultat, but inefficient in the sense, e.g., that it takes very long time to arrive at this resultat.
Brief googling for efficient selection confirms that this is often the sense in which the term is used.
Nevertheless, the third reference in the OP essentially speaks of efficiency in the same sense as effectiveness/efficacy, which is probably just poor English usage (I myself was not quite clear about the difference before reading @bob1's answer).

Thanks, so actually it will be mostly breeding vs nat. selection (the cost of time is very meta to me). Also, I would love to see Eyre-Walker's response to this answer ^^.

You have a word problem here, not really biology.
Efficacy means "power to produce the desired result/effect"
Effective means "producing the desired result", stressing the ability to produce that result
Efficiency means "degree of being efficient"
Efficient in turn means "ability to produce desired result with little waste"
Efficacy and efficiency are not interchangeable as they have different meanings, albeit a subtle difference. You could on the other hand us efficacy and effective as synonyms, though properly the synonym of efficacy is effectivness.

Appreciate the effort but I did google the definitions of the words before I asked. The problem I have is that there is no "desire" in evolution and it's hard to guess what "little waste" would mean in this context. So I think the question "What is the difference in efficacy of natural selection and efficiency of natural selection?" remains unanswered.


text:
What is this insect with scary antennae?
I encountered with this insect on the wet floor in Sri Lanka. Is it dangerous?

Yes I did it with intention to help someone who will search with the real name of that thing. (At first I didn't know it's called cerci before your answer.) I understand now its not going well with your answer however.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Can ampicillin resistant bacteria survive penicillin plate?
in my molecular bio class we were asked a trick question:
If the bacteria has a plasmid with that grants it ampicillin ressistance, can the bacteria survive if placed in penicillin?
I gave it  a thought and said that it cant, since amp differs from pen by an extra amino acid that could harm the bacteria, the answer corresponds with the class material but amp is known as the broad spectrum antibiotic.... so should i go with the  class flow  lured by the experimental assumption and assume it dies  or persist on whether it will survive? i'm really confused at this point, any input is appreciated

Neither of the two answers provided give the full answer, both touch on it, from different perspectives, but neither address it completely.
Given your description, it sounds as though the question is being asked in the context of a lab strain.
Plasmids for ampicillin resistance carry the AmpR gene on them which encodes for the enzyme beta-lactamase.
Beta-lactamase hydrolyses the beta-lactam ring, which is the 4-membered ring that has the carbonyl group and the nitrogen in the ring.
It then decarboxylates the carboxy group that results from the hydrolysis, removing the threat to the bacteria's ability to make cell walls, as Chris explains.
As both ampicillin and penicillin are closely related beta-lactam antibiotics, and have the same beta-lactam ring moiety which is the substrate of beta-lactamase, both molecules are neutralized by the enzyme and the bacterial cells will divide and not be inhibited from forming a cell wall.

The down votes without explanation make no sense at all. Both the answer that @Chris gave and the answer that I gave are factually correct. Ampicillin and Penicillin are Beta-lactam antibiotics and resistance to them is provided by the beta-lactamase enzyme. As the question said plasmid and not F-factor, we talking about transformation and not conjugation. In the lab, you use a Plasmid with AmpR to confer resistance, and pretty much any of the common beta-lactam antibiotics will be resisted by transformants.

Out of interest: Why the downvote? What is wrong with this answer, what needs to be changed?

Short answer: Your assumption is wrong and bacteria, which are resistant to penicillin are are also resistant to ampicillin.
Long answer: There are different classes of antibiotics, which have different mechanisms of action. Penicillin (and also ampicillin) belong to the class of beta-lactam antibiotics which are an irreversible inhibitor of the bacterial transpeptidase, which is needed for the proper formation of the bacterial cell wall.
There is a number of different natural occuring penicillins as well as some which have been generated by modifications of the general structure. The general chemical formula for these is shown below (from the Wikipedia article), the different penicillins differ only in the "-R"-group shown in the molecule (in the upper left):

If you now compare Penicillin G (which occurs naturally and is still used) and ampicillin side-by-side, you will see the the difference is not very big, basically only one amino group:

Penicillin G on the left, Ampicillin on the right.
The difference of this one amino group makes ampicillin more polar and allows it to penetrate the cell wall of some gram negative bacteria (the main action goes against gram positive bacteria).

The down votes without explanation make no sense at all. Both the answer that @Chris gave and the answer that I gave are factually correct. Ampicillin and Penicillin are Beta-lactam antibiotics and resistance to them is provided by the beta-lactamase enzyme. As the question said plasmid and not F-factor, we talking about transformation and not conjugation. In the lab, you use a Plasmid with AmpR to confer resistance, and pretty much any of the common beta-lactam antibiotics will be resisted by transformants.

Out of interest: Why the downvote? What is wrong with this answer, what needs to be changed?

My first reaction to your question was that it would depend on the mechanism of resistance. As Chris pointed out, ampicillin differs from penicillin only by the addition of an amino group on the amide alpha carbon. While the similarity may suggest that resistance to one confers resistance to the other, the amino group does provide a means to distinguish between the two and, through the happenstances of evolution, I could imagine cases where bacteria evolved resistance to one antibiotic while remaining susceptible to the other. This paper describes penicillin resistant but ampicillin susceptible Enterococcus faecalis strains isolated from clinical samples. While this describes somewhat of the opposite scenario as your question, I don't see any reason to say unequivocally that ampicillin resistance implies penicillin resistance.

For lab strains, with the AmpR gene encoding beta-lactamase on a plasmid it does, and based on the wording of the question I am going to say that it is referring to lab strains on to Amp or Pen plates.. The article you linked to does not give an explanation of the method of resistance. It could very well be that these bacteria have a different form of resistance than beta-lactamase, and it could be that ampicillin greater polarity, as Chris pointed out, makes it more effective against these bacteria.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Difference between negative allosteric regulation and non-competitive inhibition
Both connect to some site other than the active site which controls the shape of the active site and causes the enzyme to be less active. So what is the difference?

For allosteric inhibition, the inhibitor binds to the enzyme and induces a change in the conformation so that the substrate cannot bind anymore. The binding site for the allosteric inhibitor is different from the substrate, see the image for illustration (from here):

In non-competetive inhibition the inhibitor also binds to the enzyme indepently of the substrate (wheter it is bound or not) and does not influence substrate binding. What is influenced is the activity of the enzyme, when the inhibitor is bound, it will not process the substrate. See the figure (from here) for illustration:

So in allosteric inhibition what's changing is the affinity to the substrate, and in non-competitive inhibition what's changing is the ability of the enzyme to carry on with the reaction. Got it.

@A.Steiner no. The difference is that in allosteric inhibition, the inhibitor does not bind to the active site but to some other site in the enzyme which, due to change in enzyme structure, leads to change in activity.

@A.Steiner No. In allosteric inhibition the conformation of the enzyme is changed so that the substrate cannot bind anymore. In non-competetive inhibition the substrate binding is not affected.

@WYSIWYG, I pretty much believe that both of them (allosteric/non-competitive) bind to a regulation site which is not the active site, change the enzyme conformation and lead to change in activity.

@Chris, an allosteric regulator changes the conformation of the active site, but with saturation of substrate I know the enzyme suppose to work as there is no regulation at all - changes the affinity to substrate (Km) and not the ability of the enzyme to work (Vmax). in that perspective it's dynamics behave like a competitive inhibitor. In non-competitive inhibition, the enzyme will not work the same no matter how much substrate there is. Meaning the effect is not on affinity, like you said. The enzyme structure must be changed though (CoE/critical amino acids) in order for it not to work.

@A.Steiner a non-competitive inhibitor binds to the active site (not necessarily the substrate binding site); it may or may not change the conformation of the active site. Allosteric term itself implies "other site" and the only way by which an allosteric regulator can affect the activity of the enzyme is by changing the latter's conformation. If you don't want to believe this then I cannot help.

@WYSIWYG this is from Wikipedia - "It is important to note that while all non-competitive inhibitors bind the enzyme at allosteric sites (i.e. locations other than its active site)—not all inhibitors that bind at allosteric sites are non-competitive inhibitors". If it is not the substrate binding site, it is not the active site. Active site - "the active site is the region of an enzyme where substrate molecules bind and undergo a chemical reaction"

@A.Steiner As a molecular biologist I cannot agree with this Wikipedia article that is not properly referenced. First of all, active site is not just the substrate binding region, it is the region of the holoenzyme which is directly involved in catalysis. A non-competitive inhibitor binds somewhere in the active site (including cofactor) and prevents catalysis. An allosteric regulator (can be an activator too) bind at some other regulatory site. All these definitions are historic. We can extrapolate that allosteric regulators affect enzyme catalysis by causing overall change in structure.

There Are Two Similar but Distinct Types of Noncompetitive Binding.
Starting from a pharmacological perspective, there are 2 definitions of "noncompetitive" binding that have similar macroscopic effects but differ slightly in their molecular mechanisms. Depending on which definition you use, noncompetitive ligands can bind either orthosterically or allosterically. Aspirin at cyclooxygenase and alanine at pyruvate kinase have both been referred to as "noncompetitive" (see below), despite aspirin binding orthosterically and alanine binding allosterically. Both types of inhibition involve depression of the maximum response, efficacy or enzyme activity. In other words, they reduce $y_{\mathrm{max}}$, $E_{\mathrm{max}}$ or $V_{\mathrm{max}}$. This is described in (Lippincott. (2015). Illustrated Reviews Pharmacology. 6th ed. p. 34). Similarly, (Goodman and Gilman. (2011). The Pharmacological Basis of Therapeutics. 12th ed. p. 46) gives an operational definition of noncompetitive antagonism as that which depresses the maximal response to the agonist but the molecular mechanism of action "really cannot be inferred unequivocally from the effect". The two types of noncompetitive molecular mechanisms are (1) irreversible antagonism and (2) allosteric antagonism. Lippincott claims that both of these mechanisms are "noncompetitive" antagonism. Textbooks trump Wikipedia on credibility so I'm afraid to say that Wikipedia may have been leading people astray for years by saying that noncompetitive ligands can only bind allosterically. Due to this confusion, I think it's better to avoid the term noncompetitive entirely and opt for "insurmountable" inhibitor if the mechanism is unknown, or "irreversible/allosteric inhibitor" if the mechanism is.
Type 1: Irreversible Antagonism
Goodman and Gilmans' definition in the previous paragraph notes that the effect is for "a slowly dissociating antagonist" (i.e. an irreversible antagonist). This is mirrored in (Rang and Dale. (2015). Pharmacology. 8th ed. p. 11) and (Katzung. Basic and Clinical Pharmacology 11th ed. p. 31), which define noncompetitive antagonism as irreversible antagonism. Rang and Dale also makes the point that the term is ambiguous with other meanings of noncompetitive. Rang and Dale claim that aspirin is a noncompetitive antagonist at cyclooxygenase. It may be an irreversible antagonist but it's certainly not an allosteric one, as it modifies the orthosteric binding site. Another "noncompetitive" drug in this class (according to Rang and Dale) is phenelzine, which irreversibly binds MAO.
Type 2: Allosteric Antagonism
Not to be confused with negative allosteric modulators, (Goodman and Gilman. p. 46), (Rang and Dale. p. 17), (Lippincott. p. 34) and (Katzung, p. 32) all give a second definition of noncompetitive antagonism as antagonism at an allosteric site. This antagonism may be reversible or not but as the agonist can't displace the antagonist, it is insurmountable in all cases. Rang and Dale give the example of ketamine at the NMDA receptor, which depresses the maximal response by binding in the channel (an allosteric site) but doesn't bind irreversibly. For ligands relevant to enzymes, alanine and ATP allosterically (yet reversibly) bind pyruvate kinase. So this would cause insurmountable inhibition of pyruvate kinase activity but not irreversible inhibition. Various authors, such as (Mustafa and Hochachka, 1970) refer to this as "noncompetitive" inhibition.
Interestingly, I can't find any exogenous ligand that is both reversible and allosteric. It seems that allosteric antagonists are more relevant to receptors and transporters than enzymes. To make it even more confusing, Katzung claims that benzodiazepines (BDZ) act noncompetitively, since they bind allosterically. But this doesn't fit with any other definition of noncompetitive binding since BDZ is a positive modulator. Also interesting is that hexamethonium at the nAChR fits the definition of "noncompetitive", regardless of which one you use. It is an irreversible blocker at an allosteric site.
Marangoni, on p. 70 of Enzyme Kinetics: A Modern Approach, also points out the difficulty in distinguishing between irreversible orthosteric and reversible allosteric inhibition. Using an irreversible inhibitor is equivalent to removing some enzyme from the system, so $V_{\mathrm{max}}$ drops. But at the same time, an allosteric inhibitor causes insurmountable inhibition (reduces $V_{\mathrm{max}}$). Neither type of inhibition alters the affinity of the substrate for the active site of the enzyme (apart from the irreversibly inhibited enzymes with no affinity) so $K_m$ is left unchanged. The figure below, from (Jahangirvand et al., 2016), shows the antagonism of catalase by cimetidine on a Lineweaver Burke Plot. A glance at this graph tells us that $V_{\mathrm{max}}$ is depressed, while $K_m$ is unchanged, so we could (arguably) call this noncompetitive inhibition. But this would not tell us the molecular mechanism of the inhibition.

This is a well written and researched answer. Thanks comments are discouraged but this answer deserves credit!

Anyone reading this article should note that the IUPHAR published a standardisation of terminology which settles the dispute. I'll change my answer in due course.

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


text:
Why does the human brain not overfit when training at some task?

One of the problems that occur during (artificial) neural network training is called overfitting. The error on the training set is driven to a very small value, but when new data is presented to the network the error is large. The network has memorized the training examples, but it has not learned to generalize to new situations.

The human brain does not overfit when training at some task, but becomes better and better instead. Why? Or conversely, why do artificial neural networks overfit when are trained too much, in contrast with the human brain?

What do you mean with "over fit"?

@AliceD Overfitting is when an artificial neural network captures too many extraneous features of the data during training so that generalization becomes nearly impossible.  It's an interesting question, but it's unclear, I agree with both of you.

(parenthetically, I'm not convinced that we don't "overfit" at times, especially in the developing brain, but analogies between ANNs and BNNs are often stretched to the point where such shared features become muddled)

@jonsca - aha, interesting stuff, I never heard of this!

@jonsca - hopefully OP clarifies the question, I am getting curious :)

@emanuele It seems we edited at the same time. Feel free to revert my edit and/or make any changes you want.

@posilon your english is 1k times better then mine :)

any answer at this point would be a speculation...be prepared to be disappointed!

I'm voting to close this question as off-topic because this is not so much of a Biological problem, would be better suited to CogSci SE

I would say the human brain overfits all the time! Gambling addiction,  superstition and anxiety disorders are all examples of overfitting. We are optimized for seeking patterns and avoiding threats. Our brains mess this up all the time! But having said that, one of the major differences between the human brain and a neural network is the amount of information that's being supplied. Neural networks overfit in part because of limited data sets. Our brains have nearly unlimited data sets available, and this provides us at least the opportunity for some self correction.

Do you think that since human brain works on a reinforcement learning basis, this is another factor that outperforms supervised learning in ANN regarding issue of overfitting?

@Shelly DeForte Well, forget for a moment such complex behaviors. At simple classifications  tasks, human do not over fit. Or I am wrong?

I'm having trouble thinking of a good side by side comparison. The problem is that we're actually pretty terrible at most things you might use an ANN for because we can't really hold more than a couple of dimensions in our minds at a time. Can you give me an example of a simple classification task that a human outperforms on because the ANN is overfitting and the human is not?

characters recognitions...

I don't think we're better at character recognition because we don't overfit. I think we're better at it because our architecture is immensely better for shape recognition and differentiation. But I admit I don't know how ANNs do character recognition, so I'm not sure what the differences are.

In this fascinating talk by Geoff Hinton, there is the strong implication that the human brain doesn't overfit, because it implements a version of dropout, i.e. of randomly leaving out signals to prevent coadaptation between neurons.
Dropout has been found to be extremely effective in combatting overfitting.
Basically the idea is that the human brain has a stochastic activation of neurons, which is pretty similar to the dropout technique (except that dropout is usually done with the same probability for each neuron).

Like any statistical learner, the human brain surely experiences overfitting. You can convince people of lots of things that aren't true by showing them biased examples.
That said, don't forget that the tasks by which we judge artificial intelligence are largely defined by what human brains happen to be good at. That's part of what makes us call it "intelligence" instead of just high-performance computing.
In other words, in your character recognition example, don't forget that the character system was developed by humans. Presumably we converged on systems of characters that our neural architectures are good at recognizing and discriminating. And in general, the computer vision tasks that we consider "intelligent" often match tasks that our brains and visual systems have evolved to do well.
So, in a sense, the concepts and tasks that serve as our tests are also inherently "overfit" to our brains.

I'm confident we now have a good hypothesis on this topic: dreams are constantly working to reduce the overfitting and improving the generalization. https://www.sciencedirect.com/science/article/pii/S2666389921000945
If this is true, dreaming should be present in much more animals than we currently know.


text:
How to understand certain protein names
I am looking for a reference to help me understand what is meant by acronyms such as : H3K9me1, H3K9me2, and H3K9Ac.
I know that these are all histone proteins, but is there a general nomenclature algorithm for all cellular proteins? Are H3K9me1 and H3K9me2 just different proteins that methylate the same region? What is meant by H3K? Etc.
Thanks!

For H3K9me1:

H3: name of the histone
K9: amino acid and position (K = lysine, position 9) of modification
me1: modification (me = methylation, ac = Acetylation), and number of modifications

So H3K9me1 means that the 9th residue (lysine) of histone H3 was monomethylated. Similarly H3K9Ac means that same residue was acetylated.
Wikipedia gives a decent explanation of the nomenclature of histone modifications, and there is also a more detailed table in Nature Structural & Molecular Biology.

Thanks! This is great, now when we say H3K9me1 vs. H3K9me2, is there a different protein that performs this single vs. double methylation, or can chIp-Seq or western blotting techniques somehow differentiate between when the same protein adds one or two methyl groups?

@NaiveHalmos I don't know offhand but there are a number of histone methyltransferases (see https://en.wikipedia.org/wiki/Histone_methyltransferase). It looks like there are a number of methods to differentiate between different modifications, e.g. see http://www.ncbi.nlm.nih.gov/pubmed/22130888

There is also a cool table at Cell Signaling Technology's website that lists all the known or suspected histone modifications, the modifying enzymes (again, if known), and known or suspected functions.

@NaiveHalmos if an appropriate reagent is available, yes you can differentiate between mono-, di-, and tri-methylation by Western or ChIP/ChIP-Seq. My lab uses a lot of CST's stuff, so I know they have a bunch of specific antibodies, but I'm sure other vendors do as well.


text:
Is this species a variant of a red flour beetle?
Found this little guy crawling around the back garden - South Coast of the UK.

The closest things I could find online (with an admittedly weak knowledge of where to look up these things, aside a google search for red beetle) were the red flour beetles. However, it doesn't look quite like what we had, this being more stockier, with a dark head, and more splayed feelers.

This does not look like a red flour beetle, but more like some species of Melolontha, possibly a cockchafer. For more specific information, we would need to know, where your back garden is and maybe something to scale the bug. I would go for Melolontha melolontha, the common cockchafer.
Of the two other european species of Melolontha, M. hippocastani usually has a black edge of the elytra (see this picture), which this one doesn't seem to have, and M. pectoralis is very rare and mostly (only?) found in Germany.

I've added some location information - meant to in the original post, but forgot! But I'm on the south coast of the UK

Then it is from my understanding perfectly normal environment for a Melolontha melolontha.

M. hippocastani usually has a black edge of the elytra (which this one doesn't seem to have), which makes M. melolontha even more likely. M. pectoralis is very rare and mostly (only?) found in Germany. I've added this info to your answer and hope you are fine with this.

I totally agree with skymningen, definitely a cockchafer


text:
Why don't rats have a gallbladder, unlike other rodents?
It has long been known that rats do not have a gallbladder, though other species including humans, monkeys, cows, reptiles, dogs and mice, all have a gallbladder.
In this paper from almost 100 years ago, scientists were studying what differences the presence or absence of a gallbladder gives the composition of bile. The authors found (what we now appreciate very well) that bile from mice who have a gallbladder was much more concentrated than rat bile - i.e. one of the functions of the gallbladder is to concentrate bile.
I know this is a very speculative question, but is it known whether having or lacking a gallbladder confers some sort of evolutionary or biologic advantage (or disadvantage)?

It is perhaps worth noting that rats aren't unique in this respect. Although most rodents and lab mice species have a gallbladder, there are other rodents (e.g. species of mice and gophers) that lack a gallbladder. Equines, most camelids, cervids, cetaceans, and many birds also lack a gallbladder.

@HarryVervet completely agree - thanks for including these other species. It seems so random that some species have a gallbladder and some do not.

Just providing a possible thought here: it might also be worth considering that the disadvantage of having a gallbladder includes the potential development of life-threatening diseases in the gallbladder. Infection of the bile duct, duodenum or pancreatitis can occur due to the formation of gallstone, which is formed from bile components. Having a gallbladder allows bile to concentrate, possibly increasing the risk of developing gallstone-induced diseases.

You only need a gallbladder if you have a diet rich in concentrated fats or engage in binge eating (aka most carnivores), otherwise the liver can produce bile on demand just fine. leaf herbivores and other animals that eat low concentrations of fat or forage continuously like rats don't need the gallbladder.

Just a thought: A gallbladder not only has advantages. For example if humans contract Salmonella infections some get chronic infections. And "excrete" (life)long these bacteria with their faeces. And as a matter of fact its the gallbladder where the Salmonellae are nesting. Maybe this could be a reason why it can be advantageous to have none, especially when you have an urban rats diet?!

There are many different theories on this aspect of evolution, some of them are proved and others are just conjectures. Materials and research in this particular aspect is very few. Here I tried to provide an answer in reference to the particular animal you mentioned, i.e. rat.
Rats don't have a gallbladder possibly due to the following reasons -

The concentrating power of bile in rat's liver is high, so the main function of bile concentration by gallbladder is unnecessay in them. This is probably the most supported theory regarding this.
Rats frequently take their food so they require a continuous supply of bile. This eliminates the necessity of bile storage.
Harbivore animals relatively lack fat in their food. This reduces the need of large amount of bile salts in the intestine.

References -

https://theparadigmshiftgroup.com/animals-no-gallbladder/
Zoology textbooks
http://www.sciencedirect.com/science/article/pii/S0375090613000323?np=y

As I understand the main purpose of the gallbladder is to ensure the full digestion fatty or otherwise difficult or complex foods to digest in support of the liver.
Both rats and mice breastfeed for about the same amount of time 4-5 weeks.  but mice don't have gallbladders; it's likely not a simple matter of ingesting less fat in their diets. Most mammals including humans developed gall bladders through evolution to aid in the digestion of fatty diets into adulthood.  Rats instead developed larger cecum for the slow digestion of seeds and grains, which works in them because of their very specific gut microbiome.
http://www.drturumin.com/en/GallAcids_en.html
**http://www.differencebetween.net/science/difference-between-a-human-digestive-system-and-a-rat-digestive-system/

Please give the answer directly and provide references for it rather than giving a reference instead of an answer.

It's probably due to the fact that rats have an usually "harder do digest" diet. A gallbladder means a source of extra bile at the time of digestion. As you said mice have one but smaller, possibly rats used to have one of the same size, but as they adapted to urban live, bigger ones became advantageous.

Any sources you can add to this?


text:
How does glucose delivered intraperitoneal (i.p.) get into the peripheral circulation?
Intraperitoneal delivery of drugs or fluids is something that occurs much more frequently in veterinary medicine than clinical medicine. In veterinary medicine or scientific studies using animals, compounds are frequently given via this route that it is typically referred to as "i.p. injection" or "i.p. delivery".
When glucose is delivered via this route (by injection or catheter directly into the peritoneal space), how does the glucose actually get into the systemic circulation? That is, where does it actually go anatomically?
I can't find much data on this or an explanation that is collectively agreed upon. In particular for drug studies, some people say that the drugs or metabolites get into the portal circulation of the liver, while other people say that the drugs are absorbed by the peritoneum and enter the systemic circulation via the lymphatic system? Some individuals would argue that substances diffuse across the peritoneal membrane and then make their way into the interstitial fluid first, and then passively diffuse into the body's fluid compartments. Could it be another route? Could it be an active process or is it completely passive? Or, alternatively, could it be a combination of several of these processes?

Just a guess (which is why this isn't an answer), but I would suspect that the mechanism strongly depends on the compound(s) being injected. For example, small molecule drugs may be much more likely to diffuse across membranes than to require some sort of active transport mechanism. However, some proteins such as antibodies can usually get into the peripheral circulation fairly easily, whereas other proteins cannot (personal experience).

@MattDMo most definitely and worthy as an answer. This question is too broad imo. By adding a compound, or class of chemically related compounds will make it better answerable other than with an "it depends" answer. As of now MattDMO 's comment makes a fine answer.

@MattDMo agree with your comment above... but I want to find evidence of the actual route that a compound like glucose would take to get into the peripheral circulation - like when we inject mice i.p. with a glucose solution for a glucose tolerance test - the glucose molecule diffuses across the peritoneal membrane, but then where does it go? Does it just diffuse into the capillaries and then diffuse into the hepatic portal circulation? I don't know where to find that information - a lot of people refer to that as "common knowledge" - but that must be cited somewhere

@Christiaan - thanks for your comment - will change to glucose specifically  to address your concern.


text:
What functions other than spore dispersal does a fruiting body serve in a mycelial network?
I'm not exactly sure if this is the appropriate forum to ask this, so apologies in advance.
My question is both technical and general: what are the less obvious functions that the individual mushroom might serve in a network of mycelia. My knowledge of biology is pretty limited but I know that, for example, some mushrooms absorb radiation with some effects on the underlying network or that the network might generally shift itself underground overtime based on the signals that the individual fruiting bodies "gather" over their above-ground lifespan on.. whatever, humidity, predators, other conditions of relevance.
This is not to mystify it too much, but i'm really interested in the biological dynamic where a "node in the network" contributes something to the decentralized network, this probably sounds familiar, fungi are just the most obvious example. I was wondering what would be the term for this to begin with if there is one and if somebody could point me to some work on it at any level of resolution: from ecology to genetics or mathematics.
Thank you very much.

A cheeky answer would be that for poisonous mushrooms, the fruiting body provides vomit, faeces and corpses for nutrients.

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


text:
When does LH surge actually occur?
I’ve seen many textbooks saying that LH surge occurs in the Follicular phase while others say it occurs in the Ovulatory phase.
I’ve tried googling this, only to end up knowing two things:
1) It occurs 2-3 days before ovulation and 2) It occurs in Ovulatory phase.
Doesn’t that two contradict each other?
If you see the hormonal variation graph, LH surge occurs somewhere between follicular phase and Ovulatory phase. This is quite confusing.
So, at what phase does LH surge actually occur?

Some graphs about the ovarian cycle mention only the follicular phase and luteal phase, and the ovulation just as a point in time, not a phase, for example, here:

Source: Differencebetween.com
In this case, the LH surge starts in the follicular phase and peaks at ovulation or shortly before it.
Some other graphs also show the "periovulatory" phase (or "ovulatory phase" or just "ovulation" as a phase):

Source: Nature - Scientific Reports
In this graph, LH surge starts few days before ovulation, so in the follicular phase and peaks in periovulatory phase.

The first half of the menstrual cycle is comprised by the menstrual
  and follicular phases during which time estrogen levels are low
  (menstrual phase) and rise (follicular phase) and ends with the
  periovulatory phase in which follicular stimulating hormone (FSH) and
  luteinizing hormones (LH) peak.

Now, these graphs are still confusing, but Merck Manual defines the ovulatory phase by the surge of LH and FSH:

The ovulatory phase begins with a surge in luteinizing hormone and
  follicle-stimulating hormone levels.

In conclusion, LH surge occurs in the ovulatory phase, if the source mentions it as a separate phase, and if not, it occurs in the follicular phase.

This pathway makes more sense when viewed in an evolutionary context.  Many other animals experience induced ovulation, where various stimuli associated with copulation triggers the release of the egg.  For example, in fish and cats, the male may bite the back of the female's neck to help induce ovulation.  Whatever stimuli are received, they are pieced together by neurons that respond by secreting GnRH from the hypothalamus.  GnRH is routed via the hypophyseal portal system (a blood vessel) directly to the anterior pituitary to trigger LH and FSH production.  So what in humans seems like a slow and cyclic hormonal cycle is adapted from a rapid reflex response to sensation.
As a result, the LH and FSH surge does occur very close to the end of the follicular phase.  It has the 'intended' result of causing ovulation immediately afterward.  The follicle bursts, the egg is released, and by definition the part that remains is the corpus luteum - so the physical act of ovulation starts the luteal phase.
I see there's a rule about citations: see
https://en.wikipedia.org/wiki/Induced_ovulation_(animals)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6101186/
http://www.ansci.wisc.edu/jjp1/ansci_repro/lec/lec_25_dog_cat/lec25out.htm


text:
Photosynthesis in Higher Plants
Q:Photosynthesis in C4 plants is relatively less limited by atmospheric CO2 levels because: 1) Four carbon acids are the primary initial CO2 fixation products 2) the primary fixation of CO2 is mediated via PEP carboxylase 3) Effective pumping of CO2 into bundle sheath cells 4) RuBisCO in C4 plants has higher affinity for CO2.    Now the correct option is 2 but can you explain the reason for not choosing 4th option?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For "homework" questions, you are required to show your attempt to answer the question and to use the "homework" tag. ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

If that is the case, why would C4 plants make PEPcarboxylase the primary acceptor instead of RuBisCO? Since it is not so, C4 plants were forced to take this alternative and make RuBisCO confined only to the bundle sheath cells. The problem in C3 was photorespiration, since oxygen used to competitively inhibit the uptake of carbon dioxide by RuBisCO. Hence it turns out that RuBisCO has more affinity for oxygen. If RuBisCO had more affinity for CO2, C4 plants would not have required to take the alternative pathway that they follow.
For the fact that why C4 remains unaffected by atmospheric CO2 levels is that because PEP carboxylase concentrates CO2 levels inside bundle sheath cells. So no matter what is the atmospheric CO2 level, the level inside bundle sheath cells remain always high and perfect for RuBisCO to act upon.


text:
Methods to evaluate gene expression
I was wondering what method should i use if i want to evaluate if a gene is being expressed or not. The first method that came to my mind was Western blot , but i don't know if i could use others.
I wanted to know if western blot , specifically , is a good method to evaluate that and , also , if there other methods equally good to evaluate gene expression.
edit : I edit my question and asked about Western Blot , specifically , and asked about more general methods do evaluate gene expression.
I don't really know why my question got down voted that much , I apologize for any inconvenient.

"Best" depends on what you are doing. For over expression of a heterologous gene in E. coli, I'm content with a dark band of appropriate molecular weight on SDS-PAGE that is not present in the control. That's certainly better than a western in this particular case.

Perfectly good question! Lots of possible options depending on cell type and whether we are interested in RNA levels or Protein levels. The question might be improved by either asking for a specific system or explicitedly ask for general methods.

Thanks @JeppeNielsen i edited my question. I also do think this is a perfectly good question.

If you really want to know if your gene is being expressed up to protein, then go with western blot. mRNA based methods are good, but they will be limited in the sense that they will not account for RNAi.
This seems to be a good reference on the subject of RNAi.

RNA based methods, while certainly useful in many circumstances, won't account for any kind of non-degradative post-transcriptional regulation.

Sorry, I should have written RNAi. Take a look here

Thanks luis. One more thing : If someone says "express" , they mean the production of a certain protein or if the protein is working properly ? I think i just got confused about this concept.

@user158657, I found some questions on SE that might be interesting for you. Please check: Q1, Q2, Q3, Q4, Q5 and Q6. I would only add that, personally, I do not think that it is wrong to use gene expression when referring to gene transcription as it is commonly used in the literature. But it is certainly inaccurate.

@user158657, you could also check these references on non-coding RNAs and epigenetics: ref1, ref2 and ref3.

GFP or other flourescent proteins fused to gene products of interest can work very well, in C. elegans changes of protein expression can be tracked at cell level in live worms.  In situ hybridisation can also be used to detect RNA expression levels of targets, in indivdual cells or in whole mounts, like commonly used D. rerio.


text:
Why is the cough reflex triggered when we hear others cough?
Very often, I see a "chain reaction" in people coughing in an exam hall. One person coughs and many follow. It's not necessarily the person closest to him who coughs, it can be someone sitting far away. This doesn't just occur in this setting but also in other situations, such as in public spaces. I was wondering if this is a reflex which has evolved over time as a means of protecting our body from pathogens and harmful chemicals in the air.

https://en.wikipedia.org/wiki/Mirror_neuron


text:
Do we have information on differential reproductive success for many species?
It has been claimed that human males have a successful reproduction rate of about 40%, whereas females have 80%. This leads to the claim that we have about twice as many unique female ancestors as male. My understanding is that this claim is based on looking at the ratio of the number of generations to our most recent female common ancestor and our most recent male one.
Do we have similar data for other species? I'm especially interested in whether there are species where the number of unique male ancestors is greater than the number of female ones. Is a role reversal, like in seahorses, is sufficient to invert the ratio? Does the ratio invert for bees and ants (species where I understand, each female mates with more than one male)?

Interesting question, but note that bees and ants are a very special circumstance where many of the individuals are of non-mating castes; it doesn't make much sense to think about their reproductive success because they aren't really participating in reproduction. My suggestion would be to leave those cases out of your consideration, or only consider the mating individuals.


text:
How does evolution get around the combinatorial problem?
Imagine a combinatorial tree showing all the possible arrangements of nucleotides. Some arrangements are functional, meaning they can be plugged into a cell and create a living organism capable of reproducing. Some arrangements are nonfunctional, meaning they can't sustain any living system at all.
In evolution, new information is created as the result of what are essentially an accumulation of copying errors. My question is, would the ratio of functional to nonfunctional arrangements have to be relatively large  so that enough genetic information can arise in response to natural selection? If so, what scientific studies have led biologists to conclude that this combinatorial space is rich with functional arrangements. If it isn't necessary please explain why.

The ratio is incredibly low with almost all possible combinations being nonfunctional. If you have, by chance, a functional combination, evolution is extremely conservative and works in a step-wise trial-and-error manner, usually not taking large steps in the space of possible sequence combinations. If no one else answers your question in greater detail, I will provide an answer in the coming days.

What exactly do you mean by "genetic information"?  Are you thinking of some Shannon entropy-type thing, or do you just mean new genetic variants that increase fitness?  Please clarify.

No, with some caveats. First, about the actual value of the ratio: it's probably tiny, with almost all possible genetic sequences failing to lead to living organisms.
Why does this not make evolution impossible? Each sequence can have billions* of neighbors in sequence space. If even a very small number of those are functional, evolution can proceed. More importantly, the functional sequences are clustered in sequence space. If you pick 3 billion nucleotides randomly, you'll get nonsense, but if you mutate a single nucleotide in a human you'll most likely get a perfectly good human.
There are interesting open questions here, though, especially regarding the origin of life, and whether natural selection tends to drive populations to regions of sequence space that are especially dense with functional sequences.
*Just looking at point mutations. Including the full mutational spectrum gives many more.

would the ratio of functional to nonfunctional arrangements have to be relatively large so that enough genetic information can arise in response to natural selection?

Evolution does definitely not explore all possible combinations of a DNA. It just try things out. Of course a new gene is not necessarily recreated from scratch. A gene often get copied and then the two copies can diverge (this is called neo-functionalization).
So, no not the all possibility space is explored but this is in no way a trouble. It is not like a mutation would cause a whole brand new sequence out ov the void and hope for it to be beneficial. A path is being taken through this possibility space.

"would the ratio of functional to nonfunctional arrangements have to be relatively large so that enough genetic information can arise in response to natural selection?"
Yes it is very large. Because most mutations are synonymous mutations.
Take a look at the part about the degeneracy of the genetic code.
Another reason, and this one only helps evolution move on is called gene duplication. Many proteins in a genome are duplicated, meaning there is some redundancy involved. If we delete one protein, the fitness of the organism may/may not be affected but survival won't be affected. One example that comes to mind is Histone H1 (because I studied about it a bit). To clearly affect a change we need to delete at least three H1 genes, any less and one of its variants act as replacements.
Bonus answer, evolution does not always lead to the best possible combination, it leads to functional combinations.

I am not the down voter. But I think the first part does nothing to explain a large fraction of functional arrangements. It merely simplifies the problem to a smaller number of arrangements, but we don't know the ratio of functional ones among these!


text:
Performing histology on undecalcified tissue
Performing histology on tissue containing calcification - without performing decalcification of the tissue - is a challenging problem. There are currently a few methods to overcome these challenges including epoxy embedment, methacrylate embedment, and stabilization of tissue followed by partial decalcification. However there are drawbacks or limitations to each method as each may require specific infrastructure to perform effectively, such as a specific style of microtome.
Besides these challenges, how might you approach sectioning of calcified tissue with the aim of preservation the soft-hard interface along any calcified region? The following are objectives and demands of a successful technique:

objective 1: perform sectioning of a tissue containing thin wall calcification while preserving the spatial arrangement of soft
tissues in the region adjacent to calcified tissue - analogous to
periosteum-bone interface

objective 2: preserve molecular composition and spatial arrangement throughout process

objective 3: produce thin sections

demand 1: limit as much as possible any decalcification of to-be-sectioned tissue

demand 2: perform technique with minimal specialty equipment

demand 3: no paraffin

I will provide an initial option to begin: Tissue will be embedded in a high monomer content neutral aqueous polymer solution and chemically crosslinked following adequate diffusion time (akin to CLARITY protocol). Tissue will be cryostabilized and placed on a cryostat near -40 for sectioning.

This seems more like a research-level question someone might spend several years developing a PhD thesis to address; the techniques you mention exist because they're the best that people have come up with. If someone came up with something better that lacked the drawbacks, that's what everyone would do instead. Have you attempted the option you propose? What happened? I think it's okay to have this question here in case someone does have an answer, but I'm highly doubtful.

I think thats the purpose of asking the question isn't it? As well, getting answers which may not necessarily outright provide a method that encompasses the objectives and demands but might provide ideas toward a successful method would still be useful.


text:
Identify an animal (Japan, urban area)
I met this animal yesterday while walking along a small river in Yokohama, Japan. It came out of the bushes some 5 meters away from me, but while I was launching the camera app on my smartphone, it already went away into a fenced area where I couldn't follow and was quite far, so these are the best pictures I could take. It seemed to have something wrong with it's fur (either molting or sick). Could be a japanese raccoon dog (a.k.a. tanuki), although the images I found on Google don't look much like it to my untrained eye (maybe because of the fur), or some kind of a fox (looked even less likely). Tried asking locals, but they tend not to know anything about animals, unless those animals are either dogs, cats or foods. So, what is this?

EDIT: the size is hard to describe, I would say, it was a bit bigger than a big domestic cat, and also had different proportions - longer body, neck and legs.

Welcome to Biology.SE! For identification questions please [edit] your post to include an estimate for the size of this mammal. A description of what you could observe about its coat/skin might also help. ——— You may also want to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I've been able to narrow it down to 3 species in Musteloidea, the weasel superfamily, but I think you observed a Tanuki that was suffering from scabies.
1) Tanuki / Japanese raccoon dog - 'Tanuki' - (Nyctereutes procyonoides viverrinus).
Visually similar to what you observed. The feet and face in particular seems to fit with a tanuki. Tanuki are often observed in urban areas in Japan and have been increasing in recent years. There are frequent reports of tanuki with scabies that have missing fur and a similar appearance:
(Google search for "tanuki" and "scabies":
https://www.google.com/search?q=%E7%96%A5%E7%99%AC%E3%82%BF%E3%83%8C%E3%82%AD
2) Common raccoon - 'Araiguma' - (Procyon lotor)
Since they were introduced in 1962 as pets, there are some wild populations in Japan, including in Kanagawa prefecture where you observed the animal.
3) Japanese badger - 'Anaguma' - (Meles anakuma)
Another possibility but I think it does not fit your observation.
There are a few other species in this superfamily but I think it is safe to exclude them due to a lack of visual similarity.


text:
Is it humane to kill fish by immersing them in very cold water or ice slurry?
I'm doing some research and advocacy for the humane treatment of wild-caught fish. Humane standards are more common on fish farms than at sea, so I am trying to identify some reasonable standards for what might be considered humane and also feasible for companies to carry out. One possible method of slaughter is killing fish through cold water exposure. Below is an exact quote from a representative at a commercial fishing company (which I won't name since I don't have the person's permission to share this quote yet). I would like to know if what the person describes might be considered humane. It's unclear to me whether these fish are actually dying of hypothermia, or if it's 'cold shock' or 'live-freezing.' I'm not even sure whether these three things are distinct phenomena, or different names for the same process.
"In regards to our fish, they are all dispatched in a method to reduce waste and limit stresses to the fish during it’s transition.  A fish left flopping on the deck ruins it’s meat and stresses the fish out enough to change the flavor of the meat.  We move the fish from the ocean directly into sub-freezing temperatures.  In the case of tuna, that means a refrigerated seawater tank, with the salmon it’s a slurry of seawater and ice.  Sardines are scooped out of the ocean in large nets and deposited into tanks of refrigerated seawater.   The cause of death is hypothermia and has been shown to have a calming effect on the fish for the brief seconds before they pass."

Hi, and welcome to the site!  It would be best if you could [edit] this with some more official sources than "a representative told me." Alternatively, an exact quote from the representative would be nice.  Thanks!

You should state if they cool the water slowly or if they change them to a freezing tank. my experience of fish is that their breathing ability would slow down in the first 5 seconds and that their muscles would start to slow down within 5 seconds, they would be confused and would have the energy to get further than a few meters, which would be the extent of their startled reaction, and then they would go rigid within about a minute.

I don't think this is an answerable question, except by (the ghost of) a fish that has undergone the process.  And then we'd have to compare that to the opinion of the ghost of a fish that has been eaten by a bigger fish...

@jamesqf — I'm not sure that is fair. At very least there is research on this subject such as this review about humane killing of farmed fish ...

@tyersome: But the point is that "humane" is a value judgement that can really only be made by the fish.

@jamesqf — Why do you say that? Humane is an english word that roughly means humans showing compassion ...

Thanks for the suggestions to clarify my question, I have edited above. Also, @jamesqf, I respectfully disagree with your line of thinking. Until the unlikely day when all animal products are abolished, humans will be slaughtering animals for consumption, and figuring out how this can be done in a way to limit unnecessary pain and suffering to the animal is of pressing importance. Surely we have some capacity to estimate and reduce the suffering of an animal.

I agree with @jamesqf that this is probably not answerable here. Biology can't answer questions about what is humane or not. It's possible that you could distill your question down to something answerable by biology, and that this could be used in an argument about humane methods, but it won't tell you whether something is humane or not.

An example of the sort of question you might ask would be to first do some research on methods of monitoring stress in fish, and then ask for a comparison of a couple different slaughter methods with respect to that measure of stress.


text:
Hippos in infrared
Watching Netflix's "Night on Earth", I discovered that Hippos, or at least some Hippos, have quite a weird appearance in infrared. They seem to be covered by IR bright spots all over their body, possibly excluding their heads.
Something similar can be seen in this video on YT starting around 0:12. The following picture is a screenshot from that video:

What's the reason for this weird pattern? Why are some spots on a hippo's skin warmer than the rest?

EDIT in response to a comment by @jamesfq:
As far as I can tell, these images were taken without the use of IR illumination. The crew in the video linked above were apparently using a repurposed military thermal imager by Selex. As far as I know, these operate without any additional illumination.

EDIT II:
@Harun suggested that this might be related to hippo sweat, which looks a bit like blood. But the images I could find (the one below is from here) do not seem to suggest that it forms spots comparable to those in the IR image. But maybe the secretion spreads around the glands it comes from and looks quite different in the IR. It also looks like they sweat on the head, which has a much more uniform appearance in the IR than the body. Of course these are all just single images, maybe not representative.

I don't remember the explanation, but there's a good description in this documentary: Inside nature's Giants:Hippo

@Harun Thanks, will try to get my hands on this.

As a comment in lieu of a speculative answer below: I can also imagine the spots are depositions from insects or secretions from glands of the hippo. I've heard of secretions that have a sunscreening function, i.e. appear black in UV. They could also attract or repel UV-sensitive insects that commonly spend time around these animals; this is not uncommon with coloration visible only in UV (e.g. dark spots that plants harbor to attract). Just expanding on the speculation... I have no good suggestion as to why there would be spots in the IR spectrum!

@SPr Hmm, that's interesting. I hadn't thought about secretions, only about this being a property of the skin itself.
No luck finding the documentary mentioned above yet...

It would help to know just how the IR photos were taken.  Are they using night vision cameras that project their own infrared light (in which case the might be just spots of different IR "colors"), or are they using the hippos' own thermal radiation?

At thermal IR wavelengths most materials have similar high emissivity especially anything organic, which suggests that the variations are more likely related to temperature than to different materials on the surface. So I'd venture a guess that it's increased blood flow near the surface, possibly due to bug bites, but it's just a guess. But what's still bothering me is that the ground is black. I'd expect the ground to be warmer and therefore brighter than the sky and trees.

Sorry I can't turn this explanation into an answer, this page seems to have it: https://www.scientificamerican.com/article/do-hippopotamuses-actuall/

@uhoh Good question regarding the ground. I asked on physics SE: https://physics.stackexchange.com/q/529616/35915

@Harun Interesting point, I remember seeing this in the zoo when I was a kid. But the secretion does not seem to form spots the size of those seen in the picture. At least in the images I could find.

@user35915 The size of the brighter spots can be misleading. If they're secretion from glands in the skin, they will spread at least a little and can be warmer than the surface of the body.

@Harun Good point, will include it in the edit.

There is research to support the idea that these are areas used by the animal to regulate its body temperature.
Citation: Schneider, Marion & Kolter, Lydia & Zoo, Cologne & Germany, & De, (2003). Visualisation of Body Surfaces Specialized for Heat Loss by Infrared Thermography. J. Exp. Biol. Quart. J. Exp. Physiol. Medicine Comp. Biochem. Physiol. A J. Anim. Science. 2068. 1727-1738.
As the researchers found using a thermal camera and imaging software, there are distinct spots that can be observed in the hippo. the authors of the above mentioned paper infer that these higher temperature areas coincide with areas of rich blood flow and high nerve innervation, used to regulate blood flow and thus body temperature.
The authors also note that similar mechanisms are present in marine animals, such as seals.

Our findings demonstrate for the first time that the hippopotamus is able to open thermal windows. They appear in all body surfaces and vary in number, size and shape. Earlier histological examinations of hippopotamuses revealed a network of blood vessels deep within the dermis, and a thin epidermis, richly applied with nerve endings [3], suggesting an underlying thermoregulatory mechanism through nerval vasomotor control of the skin through connected arteriovenous anastomoses. These are referred to as specialized cutaneous vascular structures, densely innervated by sympathetic nerve fibres which permit local regulation of blood flow [4]. Arteriovenous anastomoses have been identified as thermoregulatory structures in the skin of seals [5] and presumably represent the underlying structures for thermal windows in the hippopotamus. Elephant, rhinoceros and hippopotamus are large herbivores, live in the same climatic region, and have almost hairless skin. Elephants show a great capacity for heat loss in the ears [6]. Contrary to the rhinoceros, the hippopotamus lack sweat glands but exhibits large sub dermal glands distributed over the body which release a red secret.

Nice, thank you. I couldn't find the full text. If you have access to it, could you clarify the connection between these areas and the red Hippo sweat? It's mentioned in the last sentence of the abstract, but I don't quite get the connection. Are the glands for the "sweat" also the thermal windows or are they distinct?

Also: my girlfriend reminded me that there is also footage of a seal in Night on Earth that shows the same spots, as is mentioned in the abstract. I had forgotten about that.

Nice answer, but the reference appears to be garbled — it includes a partial email address and multiple journal abbreviations all lumped together. It would be great if you could edit that so that it is easier to find the actual paper (all I could find was a Research Gate link, which appears to be where the incorrect reference information came from ...).

Here is a link to the abstract for the paper cited, there is also a link to download the whole paper on the below web page: https://www.researchgate.net/publication/228879361_Visualisation_of_Body_Surfaces_Specialized_for_Heat_Loss_by_Infrared_Thermography

@MatthewMartin It seems that researchgate is your primary source. Not many people have an account in researchgate. Does this paper have a doi or pubmed link (check the first page of the article)? The citation is not clear as tyersome already mentioned.

Following from Matthew Martin's citations, we can infer what kind of temperature management the "biological thermal windows" are for, as they travel through 4-5 inches of fat and leather:
If the hippos dwell in 25'C to 30'C water for much of the day and night, they can waste energy warming up, energy which can be spent on growing, rearing young, defending territory.
As changes in vascular perfusion are not energetically demanding, thermal windows broaden the temperature range in which endothermic organisms can regulate body temperature with minimum costs (the thermoneutral zone), particularly by extending its upper limit. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4843926/
Hippo's have spent millions of years as a water dwelling clade, their closest living relatives being dolphins, whales and porpoises. So the hippos are equipped with radiator-valves can let them stay warm in water for many hours and stay cool on the riverbank.


text:
Is the regulation of lactose operon different between Gram + and Gram -?
I know that in E. coli the lactose operon is shut down by CAP protein when binding cAMP. Is this true also for Gram positive bacteria?

I know it's stupid but I answer my own question, for those who are interested.
It is different.  CAP protein regulates lactose operon only in Gram -. In Gram + the presence of glucose shuts down the operon with another mechanism: the TCRS that relies to concentration of fructose 1,6 phosphate.

It is not stupid to answer your own question! It is actually encouraged on every SE site :)

Its not stupid at all. You saved our time


text:
does phagocytosis dependent on opsonization?
does phagocytotic activity of macrophages and neutrophils depends on opsonization by IGg (antibody) and C3 complex,if it does, so then why macrophages and neutrophils are categorized in Innate immune defense system (despite the interference of antibody).
and if it is not dependent so why macrophages act as antigen presenting cells to make antibodies, while they lysed it and fragmented it (the pathogen) on it's surface by it's own,so what is the need for it to make antibodies while the innate system can handle it alone?

Well, phagocytosis does not depend on opsonization, but it works better with it because the macrophages can detect the intruders more easily, but the secondary inmune response with IgG depends on the work of the APC cells, so let`s say a bacteria gets in your body for the first time, it can get phagocytated by a macrophage that will after present the parts on his MHC II to start the secondary inmune response.

so what's the benefit of activating acquired immune system while the macrophages  can lys and kill it?


text:
why thymectomy doesn't lead to humoral immunity deficiency?
thymus is a place where T cells educate. in all textbooks it says if you remove thymus you will have cellular immunity deficiency. so in that case you should also be humoral immunity  deficient,then why it is only the cellular immunity which is ruined?

It depends on what age the thymus is removed. There are studies that suggest after a certain age, a thymectomy has no significant effect on the human T cell compartment.

A similar question from me. Though not happy with the answer. http://biology.stackexchange.com/questions/44103/does-atrophy-of-the-thymus-not-effect-t-cell-selection-and-tolerance


text:
how body doesn't make antibodies against adjuvants of vaccine?
we know that all antigenic molecules don't have PRR on phagocytes and so they use an adjuvant that has a receptor for pattern recognation and fuse it with in order to phagocyte the antigen-adjuvant complex and present it on MHC II molecules for antibody syntheses now the question arises the phagocytes don't know which molecule is antigen and which is adjuvant then why MHC II molecules don't present the adjuvants for antibody syntheses and make the body sensitive against adjuvant and future vaccination should not be successful because the antibody recognises the adjuvant binds with it and not letting the vaccine to be processed?

Some adjuvants are not immunogenic. See this article.

Basically, this is what is happening when you receive a vaccine.

Immunoglobulins are being made agains protein adjuvants such as flagellin
Some of the adjuvants based on endotoxins such a lipopolysaccharides are not proteins. While there are some immunoglobulins produced that detect these molecules, the majority detect proteins
Most antibodies are produced against the functional conformation of the protein, so its tertiary or quaternary structure. When polypeptides are loaded into MHC II, it is a small piece of the primary sequence of amino acids. This is used to activate CD4+ helper T-Cells.
Vaccine is given in one of three ways; subcutaneously, intramuscularly, or orally (including nasally). Most antibodies circulate in the blood until they leak out of the blood vessels at the site of an infection. Also free antibody have half-lives of between 7 to 21 days, so even if there had been IgG in the tissue from a prior inoculation, it is unlikely that any will be at the site of the new inoculation without an inflammatory response taking place.

Oral vaccines will encounter IgA molecules in the mucus, so if they were made from a prior immunization, they could opsonize the vaccine, however, it is likely given in a high enough dose that some of the vaccine will reach the antigen presenting cells.
When delivered subcutaneously or intramuscularly, the vaccine will first be encountered by the innate immune system, even if adaptive immune cells were activated in previous rounds of vaccination. It is very unlikely that IgG will be encountered at the site of the inoculation, as IgG circulates in the blood and only ever really gets into the site of inoculation or infection after the innate immune cells have initiated an inflammatory response leading to the permeabilization of the blood vessels, allowing other immune cells and immunoproteins access to the site of the infection. Either way, APCs will be taking up the vaccine before the antibodies against them can neutralize them.
It is also likely a good thing that there are CD4+ cells in circulation that recognize a sequence of the adjuvant. If the B cell phagocytoses the vaccine and adjuvant, such as with a flagellin fusion vaccine, because there was specificity for an epitope on the target protein (vaccine), then even though the B cell is not making an antibody to the adjuvant, putting the adjuvant sequence on the MHC II means that it can be activated by a helper T-cell that recognized the adjuvant polypeptide, even if there is no T-cells that recognize the vaccine.

a lot of this is "common knowledge" for those of us familiar with vaccines an the immune response.. but can you list some sources?

@VanceLAlbaugh That is going to take me a while. The answer was written completely from memory and I did not refer to any sources when writing it. That being said, that knowledge is based on extensive study and reading on immunology.

A general source would be Janeway's Immunobiology, 8th Edition. But basically one would need to read the entire book and make the various connections to how the different systems play a role in the response to Pathogen Associated Molecular Patterns, Cytokines, Antigen presentation, etc. The answer is a summary of all of that information and how it is interconnected to one another.

@VanceLAlbaugh Are you okay with Janeway... This popped up again, and I don't know whether to work on it or just delete. Also WYSIWYG is right in that there are non-organic compounds used as adjuvants...

I'm completely fine with Janeway - he was a great immunologist and had a great book - used it in my graduate immunology course. I like your answer - a good compact explanation  - nice work


text:
Species Identification : What insect is this?
I noticed this insect in the end of last December on the window of my room in Pune, India. There are at least 15 such insects on this window and 12 on another. None of these have moved even a millimeter since I first noticed them. They don't move even when the window is lightly banged. They are almost 1 to 1.5 cm in length and their tails have two ends. They are almost transparent.
Imgs:

I know that it is a Mayfly (Ephemperoptera), but I am not familiar with the mayfly families in India. The reduced wings on this individual are unusual.

More properly, this was a mayfly; it is a castoff exoskeleton from either a last-instar naiad or a subimago; many mayfly groups have only two caudal filaments as seen here, so while that detail will help in the eventual identification, it cannot be used on its own.


text:
Can the hippocampus store working memory?
I'm a little bit confused about the role that the hippocampus plays in memory.
I've heard that it stores episodic memories and then consolidates the important ones into long-term memory.
My question is: if it stores episodic memory which is a presumably pretty malleable form of short-term memory why can it not store working memory as well? Also isn't that what 'memory champions' learn to do?
Further: If this is the case then what are the functional differences (e.g. pros / cons) between this and working memory supplied by the prefrontal cortex? ...Is the prefrontal cortex memory even more malleable?

If you "store" working memory, it isn't working memory anymore. Yes, that's how "memory champions" exceed the normal capacity of working memory: they store things as episodic memories to retrieve later.

@BryanKrause Well, that's just semantics...
What I'm really interested in is if it is indeed possible to 'use episodic memory as working memory' then why doesn't the brain do this by default? What draw backs are there? And what is the default way working memory is stored?

Yes, I think your question is also just semantics. Working memory is not stored, that's what separates it from other forms of memory. If you were to store the thing that working memory contains, that would be something else that isn't working memory.

Look technically all memory is stored by definition, working or otherwise. If it were never stored it would be impossible to remember even an instant after it were created. An 'unstored memory' isn't even a memory, it's just external information that you don't know.

My question is not semantics, working memory is a faculty of the mind for quickly encoding volatile memories for short-term use. I'm asking if there are any functional draw backs of this 'episodic working memory' compared to 'default working memory'.

The hippocampus is thought to respond to information that is being maintained in working memory in other areas.  Areas that are commonly thought to maintain working memory include prefrontal cortex (reviews: Chai et al 2018 https://doi.org/10.3389/fpsyg.2018.00401) and entorhinal cortex (Fransen 2005; Egorov et al. 2002).  For example, some information about recent trajectory comes to the hippocampus from prefrontal cortex via thalamus (Ito et al. 2015 https://www.nature.com/articles/nature14396).
Critically, episodic memory is not a form of working memory.  Episodic memory refers to the content of memory, not the duration.  Episodic memory storage occurs in different brain areas at different times.  The hippocampus is specialized for rapid acquisition of long-term memories.  Look up "systems consolidation of memory".
Also to address your discussion with Bryan, the general idea is that working memory is "stored" through mechanisms other than changing synaptic weights.  For example, working memory can be "stored" through persistent activity (Sanders, et al. 2013, https://www.jneurosci.org/content/33/2/424.long) or short-term facilitation of synaptic weights (Mongillo, et al., 2008, https://science.sciencemag.org/content/319/5869/1543.abstract).  Review here: https://doi.org/10.1016/j.conb.2013.10.008

So does the hippocampus actually store any memory inside itself (even temporarily)? Also can you address the draw backs of repurposing episodic memory buffers to 'extend working memory', like memory champions do for example, (e.g. is it slower to write too?)

yes, the hippocampus stores memory inside itself.  Look up "systems consolidation of memory".

i don't believe research has been done on the drawbacks of memory champion techniques as the sample size is way too small to make any concrete statements.


text:
What is the primary purpose of the prefrontal cortex?
I've heard of many functions of the prefrontal cortex (e.g. creativity, working memory, abstract thought, inhibition, planning, executive function, etc...).
But I'd like to know what its primary function is? For example is there any one function it has which facilitates all of its other functions? Or is there a known reason why it evolved in the first place?

Sorry for being such a downer on your last couple questions here, but first "What do you think?" is kind of a flag for the opinion-based questions that are not a good fit for the StackExchange format and are usually voted to be closed. Second, why should there be a one-sentence answer to this question? "Prefrontal cortex" is just a geometric label for a region of the brain, and a pretty arbitrary one at that: it includes 14 different Brodmann areas, and Brodmann areas need not themselves even have a one-sentence function.

I can re-word it but I'm not asking an opinion. I'm asking for science's best approximation of an abstract fact. The reason I'm asking is because information concerning the prefrontal cortex seems a little bit disconnected & sometimes inconsistent.

I'd certainly expect you to get disconnected and inconsistent answers to "what's the one sentence summary of what prefrontal cortex does" because there could be so many and also because most of how the brain works at a high level of organization is not currently understood.

I just want to know what the most fundamental function it serves is.

I don't think that's a factually answerable question any more than "what is the most fundamental sandwich".

Alright... I reworded it so it is more clear what I'm asking. And also clear how the answer is not an opinion.

"To facilitate an organism's survival until it can attain reproductive success and enough to facilitate reproductive success of it's offspring in a varied and challenging environment." - What more than that are you after?

I'm looking for an answer which is as simple as possible, while still being specific enough (i.e. unique to the prefrontal cortex & without ambiguous meaning), and abstract enough (i.e. able to generalize the usual 'laundry list' of functionality people attribute to it).

Attributing purpose to the prefrontal cortex (or really to any biological part) is really the wrong way to look at things.  Ask instead what it does, how it started to evolve in the first place, how it gave the possessors of early versions an evolutionary advantage...

If you want the function of the prefrontal cortex boiled down to a single coarse approximation, the answer is executive function.  That notion of more structured and symbolic cognition encompasses pretty much all of the others on your laundry list.
As with other complex and multifunctional organs in the body, reducing the prefrontal cortex in this manner is a problematic oversimplification, in much the same way as describing the function of the mouth as "getting things in and out of the body".

hm ok fair enough

This brain region's primary activity is orchestration of thoughts, actions, in accordance to internal goals. Many authors have suggested a link between personality and functions of the prefrontal cortex.
This brain region is involved in executive functions such as planning and decision-making, personality expression, moderation of speech and language, controlling certain aspects of speech, and language.

This also looks like it could become a good answer, but in addition to what I said on your other post this is a poor question because it is opinion based (see comments), which is why it has multiple downvotes. Please consider deleting this post as it is encouraging the posting of questions that are not appropriate for this site — from How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.


text:
Why is gyrification advantageous?
Standard 'Explanation':
I've seen countless neuroscience articles and experts explain that 'cortical gyrification is advantageous because it increases surface area which obviously increases your intelligence' (e.g. this wikipedia article).
Question(s):
But this explanation is woefully lacking, why does surface area matter at all? That implies  that somehow empty space is contributing to cognition (since the alternative is that space being filled with brain matter).
My best guess:
The only guesses I have are that perhaps it functions like skip layer connections in Residual ANNs. This section of the wiki page, says it is advantageous because 'it allows neurons to be closer together' which I guess kind of corroborates my idea?
Question(s):
But it is still far too vague and speculative. Why could these same wiring patterns not just emerge within a smooth-surfaced brain without wasting space? Also, does this imply that if you got more brain matter to fill in these spaces later your intelligence would decrease?

Short answer
The structural anatomy of the cerebral cortex is closely related to its functionality. The cortex is a thin sheet of only a few cell layers deep. Expansion of processing power requires enlargement of the surface area of this sheet, and simply increasing its volume doesn't help. As a consequence, gyri and sulci developed during evolution to accommodate this restriction.
Background
The human brain is characterized by a prominent and enlarged cortex, much larger than that of other primates. This is mainly due to the great expansion of the cerebral cortex during evolution. The underlying structures have, however, remained stable (Toro et al., 2008). The cerebral cortex houses the higher cognitive functions that separates us from other animals, allowing us to reason, talk, write books, develop culture and so on. As a result, to allow the development of these higher cognitive functions in man, it was the cortex that needed expansion, and not the deeper more ancient brain structures that govern more basic needs of life (breathing, heart beat etc.).
Because the cortex forms only a thin sheet a few cells thick that overlies the rest of the brain, a solution had to be found when the cortex was expanding in our early hominid ancestors, because the whole brain did not need inflation, just the cortex. Folding of the cortex increases the surface-to-volume ratio such that an expanding cortical surface fits onto a relatively stable base.
To take this a step further - why not increase volume in order to fit those extra neurons in? Since the volume of a ball increases by a third power with radius, why on earth would nature keep holding onto increasing the surface area, and not simply inflate the cortex by enhancing its thickness?
This has to do with the fact that the vertical architecture of the cortex has remained remarkably stable during evolution. In other words, evolution of a bigger cortical area to enhance higher cognitive processes has occurred in the most parsimonious way so typical for evolution: take an existing structure and enlarge it when there is need for more.
The cortex typically consists of a thin sheet covering the brain, and is not more than 3 mm thick. The neocortex represents the great majority of the cerebral cortex. It has six layers and contains between 10 and 14 billion neurons. The six layers of this part of the cortex are numbered with Roman numerals from superficial to deep (Fig. 1). Layer I is the molecular layer, which contains very few neurons; layer II the external granular layer; layer III the external pyramidal layer; layer IV the internal granular layer; layer V the internal pyramidal layer; and layer VI the multiform, or fusiform layer (Review of Clinical and Functional neuroscience, chapter 11).

Fig. 1. Cortical layers. source: Mental Construction.
Basically, layer IV receives most input from the periphery via the thalamus (visual, auditory, tactile inputs etc.), layer II/III takes care of horizontal projections for further processing, while layer V takes care of the output (motor output etc.). This basic architecture cannot be changed easily without changing the entire core workings of the cortex. As an analogy - to speed up computers in a parsimonious way, one can expand the number of processors quite easily. Coming up with a speedier processor is difficult these days, as evolution of single processor capabilities is pretty much at a dead end.
Thus, to increase the number of cortical neurons, the cortical surface must be enlarged. As the basis (subcortical structures) remain pretty much the same, creating folds (gyri and sulci) is the best way, and perhaps the only way to increase cortical surface area.
Reference
- Toro et al., Cerebral Cortex (2008); 18(10): 2352–7

I appreciate your answer and it does help but some things I still don't understand: why has it remained so stable during evolution? And if as you say evolution likes to take something which already exists and make it larger why not do that vertically instead of horizontally?

Another possible reason occurred to me, is it because of 'brain cleaning' mechanisms when we sleep? I heard once that when you sleep the brain expands & becomes 'loose' to clean itself out. Is this true, do you think its related?

@profPlum why has it remained so stable during evolution? And if as you say evolution likes to take something which already exists and make it larger why not do that vertically instead of horizontally?: because structure is related to function. The second comment you make here seems far fetched to me. No gross structural changes happen overnight.

One last question before I accept your answer, do you suppose that if extra brain matter were to fill-in these gyres after the brain has developed that it could somehow disrupt the proper functioning of the cortex?

@profPlum I can only think of brain tumors as a practical example of your hypothetical situation. Brain tumors are bad, always, as they compete with normal brain tissue for space and disrupt its normal function  for space. This probably doesn't answer your question, but it's too hypothetical to be answered in any conclusive way.


text:
Purpose of EF1 alpha promoter
Context: I have seen promoters used to have gene therapy viruses target specific cells, so I am referring to that apparent function of theirs.
As an example I have seen GFAP promoters used for targeting astrocytes (I have seen this in many more papers but this is the first one I found on google).
I am curious what the purpose of the EF1-alpha promoter in a lentil/retro/Adeno-Associated virus for gene expression is?
It would seem that it is often used for targeting embryonic stem cells, but then I had also seen else where that "The Lenti-X Expression System (EF1α Version) enables you to produce exceptionally high titers of recombinant lentivirus for expression of any cDNA in any cell type susceptible to lentiviral transduction." This made me think that perhaps since this promoter 'targets' stem cells which later turn into any type of cell, that this quote meant that the EF1-alpha promoter can be used to indiscriminately target cells? Is this true?
Please forgive any incorrect assumptions on my part, I am a novice in this field.

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, please clarify your question. You appear to be unclear on the function of promoters (driving transcription) — they don't have any direct connection to viral targeting. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

I've heard though that GFAP promoters are used for astrocyte targeting? Is this a special case?
P.S. I have seen this done in many more papers this is just the first one I found on google.

thanks for the recommendations!

EF1-alpha is considered a ubiquitous/constitutive promoter; it is effective in all animal cells and tends to provide strong expression. Embryonic (and other) stem cells are more difficult to target than other cells because they don't express genes under the cell-type specific promoters that are often used for other populations of cells, which is why you're seeing it used specifically for that application, but that's not the only use.
You'll find a lot of the promoter information on individual commercial sites and rather than promoting specific ones I'd suggest searches like https://www.google.com/search?q=ef1+alpha+constituitive or https://www.google.com/search?q=ef1+alpha+ubiquitous - use of EF1-alpha isn't "owned" by anyone so when they say these things it's not just because they're trying to sell you on some special method of theirs, they are just using a field standard approach.

Thanks, ya I wasn't trying to 'promote' a site. I just wanted to understand their claim in the wider context of the field of genetic engineering itself.

So to clarify your saying that yes it can be used to target any cell type?

@profPlum Yes. With the caveat that any time you say "any" or "every" or "always" or "never" in biology someone will find you a counterexample (the previous sentence with "any time" in it also follows this rule). Also every species has a different EF-1 alpha promoter, and they may or may not be compatible.

Haha I think you may have stumbled upon a rule that is not limited to biology but more or less universal. In CIS it is called the law of leaky abstractions. But great that is what I wanted to know!

P.S. here is the link to what I mentioned: https://en.wikipedia.org/wiki/Leaky_abstraction


text:
Does anyone know any statistics about the rate of cell division of malignant cells?
I've tried to look online to find some statistical data about the rate of growth of any type of cancerous cells, but haven't been able to find any. Would anyone know an appropriate time period for a single cancer cell to divide? Obviously, this hugely varies with the stage of cancer and type etc., but I am looking for any acceptable figure correct to an order of magnitude.

Have a look at this post for some related information. Meanwhile, please also narrow down your question to a specific kind of cancerous cell so that the question is not broad. I don't know what is an order of magnitude in your case but the doubling time can vary from a few hours to more than a day.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!


text:
Are the lower layers of skin more electrically sensitive as opposed to simply heat sensitive?
Today while surfing I accidentally rubbed the top layer of skin in my fingertips off from friction against the surfboard.
I didn't think much of it until later in the day when I was using my laptop. I brushed against a USB peripheral (the external case of which is made of metal) which was plugged into my laptop with one of my fingertips and felt an immediate searing pain, not like a burning, but very much like electrical shock.
To verify, I quickly touched it with another of my raw fingertips and experienced pain so great that it caused me to cry out in shock. I adjusted pressure with the tip of my finger, and the more surface contact there was with my finger, the less the pain was. That is, as I pulled my finger away slowly leaving only a tiny bit of skin in contact with the metal it got EXTREMELY painful, as if the fewer the affected nerves the worse the pain.
I then touched it with one of my fingers which had somehow escaped being rubbed raw, and I felt nothing. It simply felt like normal room temperature metal (there was no noticeable heat).
This led me to believe that what I was feeling through my raw fingertips was not simply heat, but electroconductivity against which is usually protected by the outermost epidermis.
Can anyone shed some light on this?

In case this gets closed, here is some basic info, and in more detail here. The basic reason you feel more (and different) in your raw fingertip is that the protective layer of squamous epithelial cells has been removed, exposing raw nerve endings which don't get triggered when the epithelium is intact. If this is not closed, I'll give a full explanation when I have more time.

Sensation comes from receptors, and there are many different types, including free nerve endings, which are responsible for sensations of heat and pain 1. These free nerve endings can be directly stimulated by voltage. (So can other receptors, but these receptors are more readily stimulated by electricity 2.) Everything you "feel" is initially detected by your receptors and transmitted to your brain. What this means is that your skin itself does not feel anything - all sensation (through touch on skin) is conducted by these receptors.
[Most] Receptors lie in the 2nd layer of skin called the dermis, which lies under the epidermis 3. The epidermis has a few sublayers itself, including a [relatively and variably] thick sub-layer composed of cellular remnants and primarily the protein keratin 4. (All receptors lie below this sublayer 5). This layer protects the rest of your body from hazards in the environment. So to gain information from the environment through touch, your receptors have to be extra sensitive.
Now, when you blister or lose a layer of skin, part or all of the epidermis is what is usually lost 6. The net effect of this is you lose distance (and a layer of heat and electrical resistance) between your receptors and the environment - it is no longer protected by the epidermis. So your receptors will be more easily activated by stimuli - such as hot surfaces and your USB port. Additionally, fluids from your extracellular space can more easily "leak"7 and form a thin, sweat-like layer of fluid over the raw skin, which can actually enhance electrical conductivity.

As for why the smaller the contact, the greater the pain? Perhaps someone else can supplement, but my speculation is that when you apply pressure, other receptors (pressure, etc.) are also firing signals. This can cause a net dampening of heat/pain signal from the free nerve endings. Although not exactly the same process, you can think of like lessening the pain in one body part by inflicting pain in another (e.g. squeezing hands really tightly and clenching jaw after stubbing toe). When you are only slightly making contact with the port, only your free nerve endings may be firing, causing uninhibited signal. The pain may not be able to be replicated with intact skin simply because the free nerve endings under the epidermis are not firing - whatever miniscule current passing through the port cannot activate the receptors through an epidermal layer.
Again, this last part is just my reasoning. I don't think this has been studied, and there is so much variability in the human body that you would probably need a personal nerve conduction study for a definite answer to this phenomenon you've experienced.

"...you would probably need a personal nerve conduction study..." No. There's not that much variation in the nervous systems of individuals.

Btw, I'm not a neurologist, but I think your explanation is probably correct. I would liken it to, say, the same amount of pressure applied to a 1 cm^2 section of the fingertip vs. the point of a needle. The first would be noticeable, the second painful.

I don't think it's necessary to speculate about any of this, and I'm not sure what all has been done in humans but certainly has been extensively studied in animal models, I don't think speculation is necessary here.