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Are there organisms with fewer than 1000 neurons?
I'm developing neural networks comprised of just 3 to 10 layers of virtual neurons and I'm curious to know if there are any insect brains out there with fewer than a thousand neurons?

Are there any tiny creatures with small numbers of neurons?
Do neuronal maps exist for those simple nervous systems?

Rotifers have very simple brains with neuron counts in the low hundreds. unfortunately they are not all that well studied. https://academic.oup.com/icb/article/42/3/660/724027/Rotifers-Exquisite-Metazoans1

@Viziionary As an aside, note that number of neurons is not always synonymous with lack of complexity; "simpler" nervous systems in terms of numbers of cells often have more complex interactions between neurons: more bi-directional communication, multiple neurotransmitters involved, etc. For example, in most vertebrate neurons, there is a pretty clear distinction between axons (output) and dendrites (input), with a few fun exceptions. However, the distinction between axons and dendrites isn't always straightforward in a worm or insect. Good luck!

@BryanKrause The intricacies and differences between neural mechanisms for different purposes are almost infinite. Which is why I use an evolutionary model where a very extensive list of mutations can happen not only to the neural structure but also the composition and mechanisms involved with each neuron and connection individually. Turns out my code handling mutation is almost as complex and extensive as the rest of the code combined. By the way, what did you mean by "bi-directional communication"?

Cells that both receive inputs and release neurotransmitter via the same processes. This happens to some extent in vertebrate nervous systems as well, but not with the major neurotransmitter systems.

@BryanKrausen Is it like this?

@Viziionary No, between neurons; that one is about microglia. This isn't my specific area of expertise (I work with mammalian nervous systems), just some peripheral knowledge so I don't know a great source to cite, or even how well those systems are understood. I think, though I am less certain about this, that some c elegans neurons release different neurotransmitters in different contexts - that might be easier to find information about.

From a computing standpoint, trying to model with few neurons isn't necessarily the best approach. Think how our computers are built from huge amounts of virtually identical transistors to get complex behaviour. Few neurons may very well mean that the interactions between the neurons are much more complex than in a "bigger brained" organism. Think the difference between modelling a thousand identical neurons compared with a hundred neurons that each work differently (as in C. elegans). If you're trying to "evolve" a brain, don't look at "least neurons" - those are heavily optimized.

@Luaan My neural model is able to evolve to beat Super Mario Bros (NES) with only 4 layers, and less than 40 neurons. The neurons each individually mutate to take on different characteristics (action potential thresholds, refactory period thresholds, memory length, default built in memory bias, and of course network structure. Just a hand-full of neurons with relatively simple behavior replication (action potential, memory, polarization, depolarization, refactory period, etc) can accomplish fairly impressive tasks in my experience.

Oh, nevermind; I was really talking about mimicking real life; there's a lot of shortcuts you can take in a game (I've done a few worthwhile experiments), and a lot of things that would be very complex in a real organism can be very easy on a computer (e.g. some memory patterns can be built using the computer's flat memory instead of simulating in a complex network of neurons). I assumed you wanted a virtual organism with as little "cheating" as possible when asking about the "least neuron count organism", which depends a lot on the complexity of its virtual environment.

@Luaan Ah, no I'm not trying to simulate physically accurate neurons in my project, just functionally accurate (which is in itself a significant challenge)

Short answer
As far as I know, a complete neural map (a connectome) is only available for the roundworm C. elegens, a nematode with only 302 neurons (fig. 1).

Fig. 1. C. elegans (left, size: ~1 mm) and connectome of C. elegans (right). sources: Utrecht University & Farber (2012)
Background
Looking at the least complex of animals will be your best bet and nematodes (roundworms) like Caenorhabditis elegans are definitely a good option. C. elegans has some 300 neurons. Below is a schematic of phyla in Fig.2.
You mention insects; these critters are much more complex than roundworms. The total number of neurons varies with each insect, but for comparison: one of the lesser complex insects like the fruit fly Drosophila already has around 100k neurons, while a regular honey bee has about one million (source: Bio Teaching).
Complexity of the organism is indeed an indicator of the number of neurons to be expected. Sponges, for instance (Fig. 1) have no neurons at all, so the least complex of animals won't help you. the next in line are the Cnidaria (Fig. 2). The Cnidaria include the jelly fish, and for example Hydra vulgaris has 5.6k neurons.
So why do jelly fish feature more neurons? Because size also matters. Hydra vulgaris can grow up 15 mm, while C. elegans grows only up to 1 mm. See the wikipedia page for an informative list of #neurons in a host of species.
A decent neuronal connectivity map (a connectome) only exists for C. elegans (Fig. 1) as far as I know, although other maps (Drosophila (Meinertzhagen, 2016) and human) are underway.
References
- Farber, Sci Am February 2012
- Meinertzhagen, J Neurogenet (2016); 30(2): 62-8

Fig. 2. Phyla within the kingdom of animalia. source: Southwest Tennessee University College

FYI a full body simulation of the entire connectome of the c elegans - openworm
https://www.youtube.com/watch?v=SaovWiZJUWY

@StefanSzekeres To be clear, that simulation does not model the connectome or include neural activity, it is only a physics simulation of musculature. Their connectome simulation is not complete yet, as the behavior at the synapses is still not completely understood (although this link is dated it still seems to be the case according to the more up-to-date openworm.org). Not quite there yet, but it's an awesome project worth keeping an eye on. It's only a matter of time.

The organism you are looking for is the nematode C. elegans, which always has the same number of neurons, 302, and has been fully mapped, see WormWeb or you can chase original publications from there. C. elegans is particularly suited for this kind of work because it has a constant number of cells which divide in an entirely predictable order and its neurons forms predictable connections. Larger organisms, such as flies, have a variable number of cells and their neurons do not form precisely predictable connections. The immense amount of knowledge about C. elegans, advanced genetic manipulation techniques, and a transparent body also helps.
I am not aware of any insects with such small brains, even a fruitfly has several orders of magnitude more.

I've asked Is C. elegans always observed with precisely 302 neurons? Are there ever individual viable exceptions?

I believe there are types of water snail with 8 distinct neurons in a ganglia, there's a bit of information here: molluscs.at.
The cell bodies of the neurons are massive, visible under a standard dissecting microscope, so they were popular among early electrophysiologists. I guess there are probably more neurons around the snail, but it's certainly one of the simplest "brains" around...

Re: insect brain size
Following article has a good summary — in short insects' nervous systems range from 7400 to 850000 neurons:
http://blogs.discovermagazine.com/notrocketscience/2011/11/30/how-fairy-wasps-cope-with-being-smaller-than-amoebas/
There may be some hope for parasitic insects, e.g. Dicopomorpha echmepterygis where male has neither wings nor eyes, it is not inconceivable for their brains to be simpler.


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Do neurons feature a collective "resistance" to firing too often beyond the refactory period?
My understanding is that neurons are prevented from firing too often by a 2-part refactory period: an immediate inability to fire again for a period of time followed by an increased threshold for firing for an extended period of time.
My question is simply whether or not there is an additional "collective" aspect of the refactory period or other mechanism which prevents too many firing based on frequency within a period of time. In other words, the refactory period as I understand it is the same each time a neuron fires, regardless of whether or not it has repeatedly fired as often as possible for a period of time before hand. I'm asking whether there's a mechanism that takes into account how many times the neuron has fired within x timeframes collectively to prevent further firings or weakens the output, sort of like a "resistance" (in which case it would be a mechanism having more to do with the synapse than the action potential / refactory period).
Do neurons feature a collective “resistance” to firing too often beyond the refactory period?

My last question was deemed too broad and low effort, hopefully this one is soecific enough and demonstrates a reasonable understanding of the relevant concepts :)

I think this one could be answered, though again, it might be more broad than you even realize. Another benefit to doing some textbook study on your own is that you would learn some of the terminology to use which will help you search for answers on your own. A question like this should probably include terms like "plasticity" or "homeostasis" and the issues you talk about at the end are a completely different area of study than the issues you begin with. :)

@BryanKrause you're right, I struggle with lack of terminology in asking neuroscience questions, I'll have to study up. So far I've been winging it with a highschool Biology knowledge level plus some Wikipedia reading and Youtube videos lol. With that I've been able to create a neural simulation from scratch that teaches itself to play Super Mario Bros, but I'm having to go into deeper understandings to push the limits beyond that.

At some point you will have to decide if you want to get serious about learning neuroscience, or if you are only interested in machine learning. Although neuroscience is great for motivating machine learning, and there is crosstalk between the fields, they are really unique fields in their own right. There are a lot of things that biological neurons can do that no one would ever use in an artificial network unless they were specifically trying to model the biological one, and there are a lot of things that an artificial network can do that biology just doesn't.

I would also add that it is a lot simpler to teach a computer to play a game than it is to understand how exactly a person learns to play a game. :)

@BryanKrause I'm experimenting with the idea that perhaps evolution has created the best possible model in terms of dynamic capability for complex thought process - better than machine learning algorithms - and so my strategy is to model the functionality of the neuron as close as possible, requiring me to go deeper and deeper into neuroscience.

Let us continue this discussion in chat.

No there isn't. Take the case of methamphetamine for example, the more methamphetamine someone has, the higher dopamine concentration in the synapse would be. An overdose of meth is the result of TOO much epinephrine metabolized from dopamine resulting in a heart attack. So, any amount of dopamine could be released, to the point of death.

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Why do scary situations make our skin crawl? Why do we have goosebumps in such situations?
I do not see why should scary situations make our skin "crawl". In scary situations, we supply less blood to our skin (which makes it paler), so shouldn't its activities reduce? Goosebumps should take up some energy to raise the hairs. Shouldn't that energy be conserved?

Goose bumps are based on a pilomotor reflex where tiny muscles at the base of hair follicles contract, which leads to the "bumps" and also raises the hair in the follicle.
It's often explained as a vestigal reflex, dating back when our ancestors had more hair than the modern human. The "puffing up" of fur has two effects, which today still both can be observed:

Raised hair traps air in the fur, thus minimizing heat loss in the cold.
Raised hair (often combined with certain postures) makes an animal appear larger, thus intimidating an opponent or predator. This is the scenario you mention in your question.

Cats are champs at the raised hair / look large trick.

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Determining water movement in Cells with Same DPD
A cell has OP=10bars and TP =5bars .other cell has OP =15 bars and TP =10bars. DPD of both is same ie.5bars. So how do we determine in which direction water will move?
OP is osmotic pressure. TP is turgor pressure. DPD is Dossusion Pressure Deficient.

Please type the full form of those abbreviations.

@JM97 Done. All Full Forms Added.


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Why are deciduous teeth shed?
Why do we have two sets of teeth? Why do earlier shed and new teeth replace them? In humans, kids do not have any need for replacement of the teeth. Why don't the milk teeth grow themselves? Or why don't we have a set of small permanent teeth as our first teeth?

Teeth grow beneath the gums in the mandibles. They don't grow once erupted. "Baby teeth" are small to fit small mandibles; too small to be as efficient as needed for the longer life of an adult. Teleologically it makes sense to have small  teeth for the time we're small, and exchange then for bigger teeth for the rest of out lives.

@anongoodnurse And since we do not grow as an adult, new teeth are not required as mandible size is fixed! Why don't you post it as an answer?


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Why do humans find baby animals cute?
Why do humans find baby animals like cats, dogs, ... so cute?
As these are potential competitors (when grown up!) or even natural enemies (like e.g. tigers, leopards, ..), the protection instinct (reasonable for the babies of your species) should therefore not apply.
I can't imagine any reason why evolution let mankind adore foreign species that much.
Maybe only humans liking the enemy's kids survived, because they weren't killed by the baby's parents.
What is the evolutionary reason?

You might find this interesting.

Have you tried cross posting to cogsci? This question might throw up some more specific answers there.

In German we call it "Kindchenschema" which is unfortunately translated only to the more unspecific "Cuteness", but sometimes also to "baby schema". This seems to be applying to most (care taking) mammals, also over species borders. The specific looks release hormones in the adult triggering care taking behaviour. This is to ensure the babies safety. That it not only works with the own parents helps ensuring the baby is cared for even if the parents cannot do it themselves.
Interestingly, the head and eye shape seems to trigger this hormone release. And it is the same for many animals. Like always, evolution uses the same winning scheme over and over again. This is why you can get a dog to care for abandoned kittens, and why you will find those puppies ever so cute.

So, you think liking animal babies is a side effect of liking our own babies? But if this behavior would disadvantageous, it would eliminated by evolution. Remember about cuckoo, which hates foreign babies. Obviously, hormones you are speculating about, can be much more specific, causing love to own babies and hate to foreign.

The cuckoo does not necessarily hate foreign babies. A young cuckoo outcompetes its "adopted" siblings. It usually wins, because it is growing fastest. And competition between siblings is also found in humans and many, many animals. And as liking other babies might not be disadvantageous, it has not been eliminated by evolution. And, as evolution is random, even if it would be disadvantageous there is no guarantee for it to be eliminated. I am not speculating about hormones, they might not be the only factor, but they are a fact.

Where do you see competition between children, in which animals? Usually children are fighting to train, but not to kill each other. Competition is low even between adults of the same specie.

In animals having litters there is often one animal which is weakest. The siblings compete for food, warmth, safety. Competition does not necessarily mean active fiting. The weakling of a litter often dies without human interference, or is mobbed out of the group. And of course there is competition between adults of the same species. Just look at humans.

We were speaking about explicit sympathy and antipathy. Implicit degrading of weak children is not the topic.

As you cannot ask the animals about it, there is no way to distinguish between explicit and implicit antipathy. Human children, the only ones you can ask, also show both.

I can't ask them, but I can observe their behavior. If weak child died because he cannot consume food, there was no behavior, directed against him. But if child was pushed out the nest by other child -- antipathy behavior was explicit.

I have seen this "cuteness" releasing hormones statement before. Could you provide a citation?
Also, be careful about saying "evolution uses the same winning scheme over and over". Evolution generates winning things and losing things. The winners stick around sure, but that doesn't mean evolution didn't produce "losers".

@GoodGravy Of course evolution is random, but a winning scheme means that it increases fitness, otherwise it would not be winning. Therefor selection is driving to preserve the winning schemes and they are conserved during speciation events. For a publication I don't have time today, but a fast search will provide you this: http://www.ncbi.nlm.nih.gov/pubmed/19175530  I remember there was another for dog/human and something explaining cats nursing ducklings.

@skymningen I inferred that you understood evolution, but the phrasing could be tidier. I might suggest an edit. That publication is quite interesting. It says that because hormonal women respond more to cuteness and respond more to cuteness when taking hormone supplements, reproductive hormones are involved. They don't tackle the issue of cultural expectation that it is feminine to respond more to cute things. I'll dive in deeper to the data (I'm sceptical about sample size and data collection method). Either way, they present it as a tentative link, not a cause and effect.

This is speculation on my part, but it could be a sort of hard-wired biodiversity conservation.
And as others have noted, it's not restricted to humans. In fact, this "weakness" to cuteness seems to extend throughout the animal kingdom, especially in mammals. There are numerous examples in nature of one species - even a predator - caring for the young of another species. Of course, there are certainly examples of the opposite as well, with predators killing & consuming young prey on a fairly regular basis. It seems most prevalent in mammals & birds, although fish also have examples.
This "cuteness" factor may be a way of nature ensuring that not ALL young for a particular species are killed off. The reaction to young may be a way of increasing the survival odds for the otherwise defenseless babies.
With humans in particular, there is a very strong psychological reaction when faced with an infant. Even those adults who normally don't want anything to do with an infant will react when they hear (or see) an infant in distress. As a result, a baby who might otherwise die gets cared for.

This seems unlikely at best. Predators often deplete prey and starve to death, which is at odds with your hypothesis.

@MarchHo - maybe that particular area had ugly babies?

The only humans survived were those, who liked baby animals. Because that humans domesticated wolfs, horses and so on, which gave them the superiority above other humans.
UPDATE
I assume, that everything what exist, should be approved by evolution somehow. Hence, IF humans actually likes baby animals, THEN it should be approved.
So, I remembered, that humans were domesticating animals and this technology was helping them (us) to survive. Also I remembered, that domestication is usually started with adoption of animal babies. Adoption was occurring by chance, on the basis of non-motivated congenital (genetic) love to baby animals.
So, my explanation is: some of human species were liking animal babies and this caused domestication. Then domestication caused evolution advantages, and these species won the competition with other human species. We are descendants of former species and conserve our sympathies to baby animals. Those who were not liking them -- died millions years ago.

What's the relation between "like baby animals" and "domesticate other species"?

Domestication requires caring when babies. Human species, which didn't like animal babies, didn't domesticate anybody and failed competition with human species which did like babies. We are descendant of latter.

I didn't know you have edited it until you commented. Since the other person who downvoted didn't comment (what I think is bad habit), he/she will only know you've edited when he/she returns here. May take a long while. Sit back and relax.

I'm not sure that we domesticated animals because we found them cute. Could you provide any sort of citation for this? For examples, baby bears are adorable... I wouldn't stick around to domesticate it though! Finding baby animals indiscriminately irresistible, to me at least, isn't a convincing argument that it aided individual/tribal survival.


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How much natural genetic variation is there between bacteria of the same species?
There are lots of questions about how and why there is genetic variation between organisms of the same species, but I haven't been able to find a numerical value for the expected amount of genetic variation.
Let's say we have two different samples of MRSA252. We sequence these samples and get the full genomes of ~3 million base pairs each. What percentage of these bases would we expect to be different (assuming there is no sequencing error)? I figure it will be about 1%, but I haven't been able to find a source.
I'm sure the answer will depend on the specific species, but I'm looking for a ballpark figure for bacteria. An academic source would be much appreciated.

I'm sure the answer will depend on the specific species, but I'm looking for a ballpark figure for bacteria.

Yes indeed it will.  Bacteria are a huge domain of life; you might as well ask for variability between all plants or between all animals.  Bacteria can live in very different environments, and the whole things is made more complex by widespread horizontal transfer.
Still, for bacteria, you can't do much better than E. coli, and boy are they a mess.  Here's a paper from 2010 that blew my mind.  The authors sequenced 61 E. coli genomes and found:

...that any given E. coli genome sequenced will have only roughly 20% of its genes part of the E. coli core, and the remaining 80% are not found in all other E. coli genomes.

20% variability within a species.  20%, one species.  E.coli is an extreme example, but still, species is a stupid concept.  Here's a 2006 paper finding that plenty of unique Campylobacter proteins simply aren't in plenty of Campylobacter species.
On a more broad scale, here's an excellent (and free) paper you should look at.  It examines islands of "microdiversity" among various species, finding that some species are easily 50%-75% different.  A simple way to estimate this is too look at gene number for bacterial species, which should make it clear that some of these bugs vary by up to an order of magnitude.
In short: A lot.

There is a database of Multi Locus Sequence Typing (MLST) data for E. coli at http://mlst.ucc.ie/mlst/
These data are limited to sequences at seven genes: adk, fumC, gyrB, icd, mdh, purA and recA. Furthermore for each of these genes only part of the sequence (in the range 452-536 bp) is characterised.
Each strain tabulated is represented by a genotype consisting of the alleles present at each of these loci. There are many different alleles found for each locus ranging from 240 variants at recA to 431 variants at fumC.
I ran a pairwise comparison (87398 comparisons -nowhere near the maximum possible, but I didn't have time to let my script run all pairwise combinations) and found that the average total divergence at these loci was 1.3%
Although this is a very different perspective from the one described by @Amory, I think it is nicely complementary, and it reveals that even at genes shared by all strains of E.coli there is a degree of sequence divergence that is quite close to your guess of 1%.

Thanks for the resource and info, this was really helpful. I accepted the other answer because there are links to a few papers.


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Evolution of scratching
Is scratching (aka the scratching reflex) thought to be inherited from a single vertebrate ancestor or is it something that evolved several times e.g. in birds, mammals etc., i.e. is it a case of convergent evolution?
I suppose this question may be somewhat subjective (what level of scratching is homologous) but since more recently the neurochemical basis for it has become more clear namely that

a molecule known as neuropeptide natriuretic polypeptide b (Nppb) that is released by nerve cells far from the actual itch site triggers an electrochemical cascade that ultimately tells the brain it’s time to get scratching.

perhaps one can ask (the same evolution question) about the signaling cascade for itch-scratch.

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Are there specific theories as to what causes cold[-water] muscle cramps?
The field of what might cause cramps is quite contested with a lot of controversy around the heat/dehydration cramps, but I find it surprising that no specific theories appear to have been proposed (or tested) while swimming, usually in cold[er] water. There's one governmental site that does acknowledge cold and cold water in particular as a risk factor. I for one never get cramps in a pool/water over 18 degree C, but I am quite likely to get them below that, no matter what I do in terms of stretching, drinking etc. (There's one other site that mentions that "muscle spasms" occur during cold-water shock, below 15 degreed C.) Am I correct that no specific theories have been proposed or tested for cold-related cramps?

Interestingly, the cutoff temperature I found experimentally for myself is perhaps reflected in one article:

during swimming at a water temperature of 18 [deg] C, it is noted that
  esophageal and muscular temperatures tend to decrease, below 37 [deg] C. [3 refs cited for this fact]

So below 18 C water temperature it appears that consistent cooling of the muscles occurs. So I guess one could ask, equivalently, why muscle cooling [below 37 C] can lead to cramps.

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Are there five common fear responses in animals?
It's been claimed on psy SE that are five common fear responses  Fight, Flight, Freeze, Fawn, and Faint (or maybe fright, flight, fight, freeze, fawn as in a post further linked from there).
To me this classification doesn't seem well supported by animal experiments... (The poster is a certified psychologist, however). Do biologists agree with a 5F classification of fear responses?
And to make this less of a yes/no question: do biologists (commonly) classify fear responses in a more fine-grained manner (than the simple fight v flight paradigm)?
It seems to me that the 3F classification fight-flight-freeze (which seems more widely endorsed even in psychology than the 5F) has a reasonable correspondent in animal behavior. But I haven't found much biological literature discussing it as such... although it presented as such in a news/pospsci video-article in Nature. The actual paper that that video is about, presents a somewhat different 4-way nested classification :

Adaptive behavioural responses to visual
  threats fall into two general categories: those that reduce saliency to
  predators (to avoid detection), such as freezing or hiding, and those
  that enhance saliency (to avoid capture), such as fleeing or retaliatory
  aggression.

N.B., one of the review papers cited by that one does use the 3F though:

Freezing, fleeing or fighting back are general defensive responses in many taxa. These defenses are mutually exclusive, since a prey cannot
  simultaneously flee and fight, or freeze and flee. Each of these defenses by itself is rudimentary and probably cannot provide a completely
  effective means to elude predation. Freezing is efficient only if employed before the prey is spotted by the predator, otherwise the prey
  becomes a stationary, easy to catch target. In fleeing, the prey can move directly away and maximize its distance from the predator, move
  toward the predator to confine it to a single clashing point, or dodge sideways to evade the attack. Prey can also run in a straight path that is
  efficient against slow or distant predators, or in a zigzag path that is efficient when a raptor is close or fast. In all, freezing and fleeing
  constitute together a complex and flexible defensive response, and are probably controlled by different motor systems that are interconnected to allow fast switching between these behaviors, as required for an effective and versatile response.

So is there a commonly agreed classification in biology for fear responses?

After thinking a bit more about this, it's probably reasonable enough to consider "fawning", that is submissive behavior as an alternative response, with the caveat that it doesn't show up much in predator-prey contexts, but mainly in contests between sexes (usually males) of the same species. I don't know if biologists see it this way though... i.e. as related to the other responses.
And if that's not complicated enough, one author suggests "risk assessment" (behavior) as a separate part of the response repertoire (in predator-prey interactions):

In rodents, an extensive repertoire of innate defensive behaviors can be seen in predator-prey interactions in natural and semi-natural (laboratory) situations. To predator threat, rodents of small prey species exhibit a general cessation of ongoing non-defensive activities (e.g., grooming, playing, foraging, feeding and sexual behavior) in both adults (Blanchard and Blanchard, 1989) and preweanling pups (Takahashi, 1992), along with enhancement of avoidance, flight, freezing, risk assessment, defensive threat and defensive attack behaviors (Blanchard and Blanchard, 2008). Rodents will also readily bury novel, aversive, or potentially dangerous objects (Treit et al., 1981). Manifestation of specific behaviors is dependent on a number of factors: (1) context – an animal will typically flee a threat within an environment in which escape is possible, yet when trapped it will freeze; (2) stimulus ambiguity – whereas ambiguous stimuli, such as predator odors, elicit risk assessment behaviors (e.g., stretch attend, stretch approach, olfactory investigation) and are often associated with a state of anxiety, discrete, present threats elicit flight, avoidance, defensive threat and attack, and are associated with a state of fear; (3) defensive distance – the distance between predator and prey shifts defensive coping strategies from avoidance to escape, with short distances to the threat and unavoidable contact culminating in defensive threat and attack postures.

This last quote highlights something else I've been pondering, namely the difficulty in delineating fear from anxiety in animals. Depending where one draws the line between these, more or fewer responses qualify for a classification...

To add to the discussion, there is talk of a 6th response. This is a newspaper article. I will try and find the clinical psychologist's report, but may be next week before I find it

I've never heard "5F" referred to in animal behavior; this seems a bit opinion-based, though, is it not? Sort of a lumpers-vs-splitters argument. As far as fear vs anxiety, that's somewhat of a separate issue, although it is certainly of great interest especially in designing rodent experiments to apply to human psychology. From a neuroscientific perspective, though, I think fear and anxiety in rodents are considered to have the same responses, the fear vs anxiety distinction is more about context and higher order processing.


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SNP vs common SNP
Wikipedia citing Nature defines SNP to be a one where each (thus the lowest frequency) allele exceeds some percentage threshold in the population. But I see a lot of papers and books calling such an entity a "common SNP" rather than leaving it unqualified example 1, example 2. Are they using a different/simpler definition of SNP?
Another book says that "SNPs most commonly refer to single-base differences in DNA among individuals" with no qualification on frequency. So I'm guessing those two sources that define "common SNP" use this broader definition of SNP. Would anyone venture a guess which definition of SNP is more prevalent? There's no discussion on the topic of the definition itself on the talk page of the Wikipedia SNP article...

I think the convention is that a point mutation with a frequency of 1% or more of the population is a 'Single Nucleotide Polymorphism' and anything lower would be 'Single Nucleotide VARIATION'.
So regardless of the frequency, any point mutation would be a 'Single Nucleotide Variation'. At higher (more significant) frequencies, we call it a 'Single Nucleotide Polymorphism'. Some may choose to name an SNP of high frequency (for example with a frequency of 15% or more of the population) as a 'common SNP'. In reading, texts will usually give you the percentage for the SNP and their naming choice should make sense. There is no fixed systematic number at which an SNP becomes 'common' or 'rare', since anything less than 1% won't count as one.


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Why does shaving dehydrate the skin? Is there an hormonal effect involved?
I want to understand why the face becomes dry after shaving and if shaving affects hormones? I've heard that after shaving, hair grows back faster, why? Shaving damages hair follicles and they become inflamed. One could get an infection JUST by shaving because tissue is ripped from the hair follicles. So maybe the increase in hair growth can be attributed to the natural blood rush that brings nutrients to the damaged follicles when they are inflamed after shaving....

You answer your own question, there is absolutely no biological reason to shave, its social. 2) One does not control the amount of sweat one produces, I wish we could. 3) You are combining multiple questions into one, please don't and post separate questions for each query instead. Voting to close.

@terdon You represent a jaded portion of this community, you don't like my question(s)? Explain to me why it they aren't valid, otherwise you have the option of nonparticipation in this thread.

I still don't see what you're asking. Of course running a sharp blade against your skin causes irritation. Are you asking why an how does skin get irritated?

@terdon is there something happening with hair follicles? And yes, I understand how the skin gets irritated-- I want to understand why the face becomes dry after shaving and if shaving effects hormones? I've heard that after shaving, hair grows back faster, why????

Ah, then please rephrase your question to make that clear. Mention the hormones and that hair grows back faster. "Our own biology rejects shaving" is really unclear.

Hmmmm... any special reason that makes you think hormones are involved?

@nico Not in particular, but through shaving we damage tissue, which might cause an uptake in hair growth hormone. If not enough hormone is available, wouldn't the body think it is deficient in the hair growth hormone and produce more?

@Rustyn Yazdanpour: I would assume it is just a local reaction, otherwise all of your skin would be affected, which is not the case... My take (but I may be wrong) is that it is just a side effect of the inflammation (e.g. some interleukins can cause dry skin).

First of all 'Testosterone' hormone controls the growth of hair on our body and also oil secretion. Depending up on the nature of a person's body, this hormone controls the growth of the hair.
Why shaving facial hair leaves the skin dry ?
First let me explain the reason behind the oiliness of the skin. Sebum is produced by the sebaceous glands and is a complex made up of cholesterol, free fatty acids, glycerides, squalene, and wax esters. Sebum and sweat, along with the epidermal lipids discussed earlier, make up the oil on the surface of the skin. Some people will have more oily skin and some have less which depends on the nature of body.
While shaving the sharp razor cuts the hair and also damages the skin and hair follicles. The level of damage to skin also depends whether you are shaving downwards or upwards. Because upward shaving usually causes more damage to skin and hair follicle. Complete detail of damage to hair follicle can be found in this article: Science of shaving.
Shaving also removes skin lipids and water content creates pores which exposes the skin. If the surrounding atmosphere is dry then skin loses water. Or if the surrounding is moist or humid then water content will be balanced. That is the reason why we use artificial face moisturizer for immediate remedy to avoid infection and balance the wetness of face. So it takes a while for the skin to get back to normal state if nothing is done after shaving which sometime leads to acne or rashes due to infection.
Another reason for dry face is use of hot water which removes skin oil instantaneously. So lukewarm water or cold water will further reduce the dryness of the skin. (Use of shaving cream with high alkaline content will obviously result in dry skin. This holds for soaps also.)
Complete details can be found in the first link provided and Drying skin after shave.


text:
Understanding these SNP annotations
I am looking at the PharmaPGKB database for SNPs and trying to understand what the following annotation means:
rs1801131 at 1:11854475 in CLCN6, MTHFR (VIP)

Ok, the SNP identified by rs1801131 occurs in the first chromosome, at position 11854475.
Then, the two genes' identifiers come. The position 11854475 is inside the gene MTHFR. Why do they also annotate the SNP to the gene CLCN6 (which is a "neighbour" of MTHFR) ?

It is because the two genes overlap:

CLCN6 is on the plus strand and MTHFR is on the minus strand. The SNP is annotated to both because it falls in a region of the genome claimed by both genes.


text:
What is Luc Montagnier's research on electromagnetic signals from DNA about?
After reading a Youtube comment, I started reading on Luc Montagnier's research on electromagnetic signals from DNA. I haven't been able to find a source that would clearly explain what it's about. I would like to know, if possible,

what the claims are exactly;
what experiments were carried out;
whether the results have been replicated independently;
whether the results contradict anything considered firmly established scientific knowledge (it seems Montagnier says they do) and, if so, how;
what the criticism is.

I know it's a lot to ask, but if you could make your answers accessible, it would be great. Please don't refrain from using technical language where it's necessary, but do try to give a general picture for those (including me) who might not understand it.

Have you read the stuff at his webpage, where three papers on the topic have been posted: http://montagnier.org/Electromagnetic-signals-DNA?

This question is rather broad, I'd suggest to read the papers and make your question more specific. On the other hand you might not bother with this topc at all, the entire thing is complete nonsense.

@TomD Being a Nobel laureate doesn't make him immune from criticism. I read the paper a while back, and it is just extremely bad. He makes an absolutely extraordinary and implausible claim, but the experiments and setups described in the paper (rather badly and without enough detail) are prone to noisy results or contamination.

Pharyngula has a nice explanation (and a scathing criticism) here: http://scienceblogs.com/pharyngula/2011/01/24/it-almost-makes-me-disbelieve/

@TomD Karry Mullis is a Nobel laureate who believes in astrology and James Watson is a Nobel laureate who believes that black people are less intelligent than white. Having a Nobel just means you had at least one idea that a group of people considered good. It does not make you an infallible genius. Silly claims are silly claims Nobel notwithstanding.

I just read one of the articles from the site. Wow. Just wow. It is hard to give a rebuttal because they don't actually show any analyses, just some very low quality screenshots with no numbers and no stats. The images are too small to actually be readable so we have no idea what their data are. Their logic is also seriously flawed. I will try and write something up when I get the chance but really, this is pure crap. Just have a look at the image (also reproduced in the link provided by @ChinmayKanchi) and tell me if you can actually see anything.

@TomD I know, it just annoys me that people take notice just because someone has done good work in the past. Work should be judged on its merits, not the laurels of the scientist involved. What claims did McClintock make by the way? As far as I know her (wonderful) early papers were scientifically sound, people ignored her because transposons sounded weird and she was a woman. The work discussed here is shoddy, not because of their conclusions but because they have no data to support said conclusions.

@TomD Ah, so I did, and yes, I misunderstood you again. Sorry, we seem to be saying the same thing I just failed to see it. Apologies :).

@TomD I like your 'non answer' why not just leave it as one?  I remember the memory of water paper - the comparison is an apt one.

Duplicate of https://biology.stackexchange.com/questions/11121/what-is-luc-montagniers-research-on-electromagnetic-signals-from-dna-about .

I think that ymar poses an excellent set of questions that should be discussed on these forums.  It brings back memories (sic) of the memory of water controversy.
I'll quote from Andy Coghlan's excellent article published in New Scientist in 2011
Draw your own conclusions.  (The emphases are mine).

... So what have
Montagnier and his team actually found? Full details of the
experiments are not yet available, but the basic set-up is as follows.
Two adjacent but physically separate test tubes were placed within a
copper coil and subjected to a very weak extremely low frequency
electromagnetic field of 7 hertz. The apparatus was isolated from
Earth's natural magnetic field to stop it interfering with the
experiment. One tube contained a fragment of DNA around 100 bases
long; the second tube contained pure water.
After 16 to 18 hours, both
samples were independently subjected to the polymerase chain reaction
(PCR), a method routinely used to amplify traces of DNA by using
enzymes to make many copies of the original material.
The gene
fragment was apparently recovered from both tubes, even though one
should have contained just water (see diagram).
DNA was only recovered
if the original solution of DNA - whose concentration has not been
revealed - had been subjected to several dilution cycles before being
placed in the magnetic field. In each cycle it was diluted 10-fold,
and "ghost" DNA was only recovered after between seven and 12
dilutions of the original. It was not found at the ultra-high
dilutions used in homeopathy.
Physicists in Montagnier's team suggest
that DNA emits low-frequency electromagnetic waves which imprint the
structure of the molecule onto the water.
This structure, they claim,
is preserved and amplified through quantum coherence effects, and
because it mimics the shape of the original DNA, the enzymes in the
PCR process mistake it for DNA itself, and somehow use it as a
template to make DNA matching that which "sent" the signal

I always knew there was something suspect about genetics!  Stick to biochemistry, that's what I say :-)

PCR can amplify a single DNA molecules. In fact, single cell PCR is possible. So... one has to be very very careful.


text:
Ramifications and possibility of a diet consuming exclusively of human semen
Semen is a thick, nutritious liquid, rich in vitamins (such as C, B12), amino acids, lipids, monosaccharides (fructose), et cetera. Can semen's ability to fulfill the needs of human organism provide enough essential nutrients to keep the body alive and functional? And if so, would it be a healthy life?
Can a glass of ejaculate a day keep The Reaper/doctor away? If not, how long could a person survive on a "diet" like this?

Don't know why this one was down-voted. Up-voted to offset. This is a question concerning human biological processes, despite unsettling implications to some responders.

Right, I do realise that semen content varies, also, question that should have been asked is 'roughly, how long one can take that diet [I mean - is it more like 3 weeks or 3 months - or else] and what exactly is most likely to cause death'. I should be more specific. Thanks for help however, kind sir MCM - and, can't vitamin K be manufactured by intestinal flora?

@MCM it may concern human biological processes, but it's not relevant for anything. I don't see how this is any more valuable than any other "how long can I live eating only X" almost all of which are simply rhetorical "just curious" questions with nothing particularly useful about them.

I downvoted because the question as phrased is not suitable for this site. Asking "what is the nutritional content of human semen" would be more appropriate for a biology forum. In what possible context would you be confronted with a situation where you had to survive on male ejaculate?

I agree the question is not the best, but it is not a topic forbidden in the FAQ, and it is an answerable question that doesn't require an extended conversation or a book's worth of text. While it would have been nice to have the question phrased better, as Poshpaws suggested, not everyone will think in that manner - and I don't see why they should be excluded. Once a question like this has been asked and thoroughly answered, then it can serve as a reference for future questions.

The question is absurd on a number of levels, but also on the level of energetics. The expenditure of energy and number of individuals required to generate a sustainable amount would far outweigh any benefits provided and would only be the diet of the Emperor or the Pharaoh, i.e. only someone with dominion over a large numbers subjects. @MCM also left out a very obvious drawback, that seminal fluid is a vector for a host of pathogens, from HIV, Hepatitis, HPV, Gonorrhea, Chlamydia, etc.

No, you cannot live off of semen.
A source from Columbia.edu:

A typical ejaculation fills up about one teaspoon; the actual amount is determined by a man's age (younger men usually make more semen), when he last ejaculated, and how long he's aroused before ejaculating, among other factors. Contrary to what you've heard, semen is not loaded with calories. Each teaspoon of ejaculate has about 5 - 7 calories and some 200 - 500 million sperm. Since sperm make up only about 1 percent of semen, what accounts for the other 99 percent? Well, its other ingredients include:

Fructose sugar
Water
Ascorbic acid (a.k.a., vitamin C)
Citric acid
Enzymes
Protein
Phosphate and bicarbonate buffers (bases)
Zinc

Can swallowing semen enrich a protein poor diet? Unless you're gulping gallons of it each day, it's no substitute for real nutritious cuisine!

From a non-academic, but apparently well-informed source, semen contains:

Semen contains only 15 calories and boy does it have a lot of stuff in it. So let's have a look. Ejaculate contains ascorbic acid, blood-group antigens, calcium, chlorine, cholesterol, choline, citric acid, creatine, deoxyribonucleic acid (DNA), fructose, glutathione, hyaluronidase, inositol, lactic acid, magnesium, nitrogen, phosphorous, potassium, purine, pyrimidine, pyruvic acid, sodium, sorbitol, spermidine, spermine, urea, uric acid, vitamin B12, and zinc.

I've highlighted the nutritionally-relevant ingredients. You'll notice that there is some overlap - with the Columbia source. What you won't notice, though, are the rest of the Essential Vitamins and Minerals:
Vitamin A (retinol)
Vitamin B1 (thiamin)
Vitamin B2 (riboflavin, vitamin G)
Vitamin B3 (niacin, vitamin P, vitamin PP)
Vitamin B5 (pantothenic acid)
Vitamin B6 (pyridoxine, pyridoxamine, or pyridoxal)
Vitamin B7 (biotin, vitamin H)
Vitamin B9 (folic acid, folate, vitamin M)
Vitamin D (ergocalciferol, or cholecalciferol)
Vitamin E (tocopherol)
Vitamin K (naphthoquinoids)
Chloride (Cl−)
Chromium (Cr)[4]
Cobalt (Co) (as part of Vitamin B12)
Copper (Cu)
Iodine (I)
Iron (Fe)
Manganese (Mn)
Molybdenum (Mo)
Nickel (Ni)
Selenium (Se)
Sulfur (S) numerous roles[5]

I should also mention that the specific amounts of each ingredient will vary from person to person, as diet can play a major role in flavor resulting from the changed nutritional content (i.e. - higher fructose levels).
As perhaps the most reliable source I could find, there is a Wikipedia article with references concerning the makeup of human seminal fluid and has this information:

amino acids, citrate, enzymes, flavins, fructose (2–5 mg per mL semen,3 the main energy source of sperm cells, which rely entirely on sugars from the seminal plasma for energy), phosphorylcholine, prostaglandins (involved in suppressing an immune response by the female against the foreign semen), proteins, vitamin C
acid phosphatase, citric acid, fibrinolysin, prostate specific antigen, proteolytic enzymes, zinc

It echoes the other sources closely, and still yields insufficient evidence that a person could live off of semen exclusively.
As for how long you can live? From a Scientific American article concerning starvation there have been confirmed instances of hungers strikes lasting up to 40 days. Assuming you could consume enough semen to sustain your body's daily Caloric requirements, you would die of malnutrition eventually. Scurvy - the inadequate intake of Vitamin C (Ascorbic Acid) - would probably be the culprit, as deficiency becomes clinical in 1 to 3 months with the later stages of Scurvy being: "...more severe and life threatening; common manifestations include generalized edema, severe jaundice, hemolysis, acute spontaneous bleeding, neuropathy, fever, convulsions, and death."
Assuming that there is enough Vitamin C in semen, you would die of other deficiencies. Since Vitamin B1 (Thiamine) is water-soluble (is not stored in your fatty tissues), not found in semen at all, and the body only reserves about a month's worth, after 30 days you would start to experience Beriberi - which is only slightly less fun than Scurvy.

An impressive answer. However, that first constituent from the second source - "aboutonia". I can find no trace of a definition for this. All Google results seem to point back to this source, it isn't in my dictionary and it doesn't generate any hits at PubMed. Presumably it was originally "Ejaculate contains about [something].." but I can't come up with a candidate that explains the "onia"

Right, I do realise that semen content varies, also, question that should have been asked is 'roughly, how long one can take that diet [I mean - is it more like 3 weeks or 3 months - or else] and what exactly is most likely to cause death'. I should be more specific. Thanks for help however, kind sir MCM - and, can't vitamin K be manufactured by intestinal flora?

@Alan Boyd - I wouldn't be surprised if they meant albumen, or something similar. It's not the greatest source, but there weren't any "hard" sources for the nutritional content of semen like journal articles or studies. There's supposedly a 2004 study out of Sydney, but I couldn't find it.

@Arwil - Vitamin K can be manufactured by intestinal flora, yes, but not in the amounts necessary to sustain human life. My personal opinion is that you wouldn't live for much more than a month. There have been hunger strikes for as long as 40 days, but if the semen didn't contain enough Vitamin C then Scurvy would kill you in a few weeks.
Edit: Also removed "aboutonia" since it's not a real compound.

I see. So, summing up, consumption of significant amount of semen, sufficient to postpone suffering from malnutrition and scurvy, can probably lead to about 2 months of not so quality life, ending in agony of 'deficiency-based' diseases, such as beri-beri. Thanks a lot, you really did a tremendous job!


text:
Is there any plausible biological mechanism for "universally protective vaccines" via "MHC allotype-independent immune effector memory cells"?
Geert Vanden Bossche, who has recently gained some fame for dissing all current Covid-19 vaccines (and who is also asking the WHO to meet him so they can  be infused with his wisdom), has had the same poster at a couple of conferences/expos in 2015-2017. Quoting one of these (only the title seems to differ):

Universally protective vaccines: A revolution in modern vaccinology
Geert Vanden Bossche (University Leuven, Belgium; Univac NV, Belgium)
To eliminate safety risks related to infectivity, inactivated pathogens and more suitably, well-characterized pathogen-derived
antigens (Ags) have increasingly been used as immunogens in modern vaccines. The selection of these Ags is usually based on
their capacity to induce immune responses that correlate with natural protection. These Ags, however, are known to be antigenically
variable or conformation-dependent (e.g., B cell epitopes) and/or subject to immunogenetic restriction (e.g., linear, T-cell epitopes). In
addition, the immunogenicity of good vaccinal Ags is largely dependent on memory CD4+ T helper cells. However, activation of the
latter upon natural infection or foreign Ag exposure of genetically predisposed subjects can occasionally lead to immune pathology.
Priming of CD4+ T helper cells by adjuvanted vaccines is, therefore, increasingly raising safety concerns. On the other hand, Ags
that are highly conserved and vulnerable because of their exposure on the surface of infected or pathologically altered host cells are
either not immunogenic or subvert the host immune system. Hence, they are not used as vaccinal Ags in contemporary vaccines.
We consider that new technologies enabling immune targeting of these Ags by natural, MHC allotype-independent immune effector
memory cells is the new Holy Grail in modern vaccinology.

Basically, is this complete nonsense or is there any plausible biological basis for "universally protective vaccines"?
In his Covid-19 talk, he basically says that natural IgM is better than anything else, which actually seems dangerous crackpottery in the context of Covid-19 because patients with numerous but low potency antibodies are often among the dead.
But in his Covid talk he never mentions "MHC allotype-independent immune effector memory cells" which showed up as his punch line in these older posters that I'm asking about. So is this (older) concept (of his) phantasmagoric, or does it have any biological corresponded? I've looked through a review on memory T cells, which describes the effector memory as a rather problematic subset because it's apparently made of only seemingly connected further sub-types, but I can't tell if any of these could possibly have anything to do with what Bossche is saying. In particular, how would any effector memory cells be the basis for a universal vaccine?

I'd appreciate some comment(s) as to what is wrong with this q, to go along with the DVs.

"Universally protective" is the epitome of hokum; why spend energy reading any further?


text:
How do we know that the "original animal exposure event" of a human to the Covid-19 virus occurred between October and December 2019?
In a Yale med page (interview) on Covid-19 from January it is said that

The molecular dating of the virus genomes indicates that the original animal exposure event happened sometime between late October and early December of last year, very near the times that the first cases were detected. This is unlike Zika virus, for example, where transmission occurred for many months before the virus was detected.

To someone unschooled in molecular dating, how do you explain that we (seem to) know with such precision when the "original animal exposure event" occurred in that October-December timeframe?

@reuns: I'd accept that as frame challenge answer (there are some papers which say it that way, IIRC). I think for SARS it's still disputed in some corners exactly how it was transmitted to us.

From what I read in cell cultures it seems that when changing the species/cell-line the virus usually gets between 2 and 10 AA mutations in days or weeks. I think this idea deserves to be investigated a little more because if we find this mutation process usually lasts for months it would indicate that the species jump occurred a few months earlier.

Sorry, I linked to the wrong paper (in the same journal) in my previous comment. The one disputing more intensely the route of SARS to us is https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6356540/ (section 2.1)


text:
How verified experimentally is the Marginal Value Theorem for viruses?
Reading some Stanford notes on R0, they get to MVT and optimal virulence:

Consider a directly-transmitted infection from which there is no recovery (e.g., Herpes Simplex). The population experiences a baseline mortality rate, µ, and a disease-induced mortality δ. [Then the SI model]

ds/dt = −βsi − µs
di/dt = βsi − (µ + δ)i,

Figure 4: Marginal value theorem for optimal virulence. The ESS [evolutionarily stable strategy] virulence occurs where a line
  rooted at the origin is tangent to the curve that relates β to δ. Two curves are depicted. The
  first curve shows a pathogen in which transmissibility increases relatively rapidly with mortality.
  Point A indicates the optimal balance between β(x) and δ(x) under this case, and the optimal
  virulence is indicated x∗
  . For the second curve, relative transmission is less efficient. Therefore,
  the tangent line from the origin to the curve hits further out (B) along the mortality axis and
  the optimal virulence is higher (x∗∗).

Wikipedia has a page on MVT but it doesn't discuss viruses/virulence at all (although it has some criticism of MVT from other angles/domains). So, how verified experimentally is MVT for viruses?

The answer seems to be "not much". I did find one paper that proposed MVT for viruses but instead of transmission efficiency in abstract terms they used/proposed lysis time as the parameter that might get optimized for/by phages. And as dependent variable they proposed not mortality but host density.
The problem indeed seems to be that before one even bothers to consider such a (MVT) model, the assumption[s] that that parameter gets optimized need to pass the "smell test".

A fundamental issue is whether the phenotype at the
  center of an optimality model has sufficient genetic
  variation that is sufficiently unconstrained to evolve in a
  manner consistent with the model. There might be a lack
  of genetic variation in the phenotype per se. Alternatively,
  there might be genetic variation for the phenotype, but
  such variation lies in a ‘higher dimensional space’ than is
  assumed in the optimality model [32,33]. This means that
  selection acting on traits outside of the optimality model
  can drive phenotype evolution in a way that is not captured
  by the model (as proposed for the evolution of some disease
  virulence models [34]).
Lysis timing has a clear genetic basis in all lytic phages,
  suggesting that it is appropriate for optimality. Large genome
  phages have modular lysis timing genes (holins and
  anti-holins). Mutations in holins have few pleiotropic effects,
  as shown by experiments with site-directed mutations in
  holins. Perhaps more crucially, holins translocated to
  different phage genomes retain their function in the new
  genome [24–26]. These studies establish a mechanism for
  genetic variation in the optimality phenotype that is free of
  major pleiotropic effects. In essence, holins provide a genetic
  ‘identity’ for lysis time [35].
Lysis timing also has a clear genetic basis in phages with
  small genomes, because these phages have genes dedicated
  to lysis. Thus, lysis timing can plausibly evolve through
  changes in the expression and activity of the lysis genes.
  Evidence of genetic variation in the phenotype could be
  obtained otherwise (e.g. by measuring heritability in lysis
  timing). However, knowledge of genes that regulate lysis
  timing not only circumvents the need for such evidence, but
  also reveals that lysis timing is and has been a major fitness
  component in phage life histories.

Subsequently the same authors proceeded with an experimental verification in another paper

Here we employ phage mutants to explore issues of phage latent-period evolution as a function of the density of phage-susceptible bacteria. Theory suggests that higher bacterial densities should select for shorter phage latent periods. Consistently, we have found that higher host densities (≥∼107 bacteria/ml) can enrich stocks of phage RB69 for variants that display shorter latent periods than the wild type. One such variant, dubbed sta5, displays a latent period that is ∼70 to 80% of that of the wild type—which is nearly as short as the RB69 eclipse period—and which has a corresponding burst size that is ∼30% of that of the wild type. We show that at higher host densities (≥∼107 bacteria/ml) the sta5 phage can outcompete the RB69 wild type, though only under conditions of direct (same-culture) competition. We interpret this advantage as corresponding to slightly faster sta5 population growth, resulting in multifold increases in mutant frequency during same-culture growth. The sta5 advantage is lost, however, given indirect (different-culture) competition between the wild type and mutant or given same-culture competition but at lower densities of phage-susceptible bacteria (≤∼106 bacteria/ml). From these observations we suggest that phage displaying very short latent periods may be viewed as specialists for propagation when bacteria within cultures are highly prevalent and transmission between cultures is easily accomplished.

In the same vein, there's a later paper titled "Bacteriophage Adsorption Rate and Optimal Lysis Time".
There might be more papers like this, but it doesn't look like the (more) universalist approach (i.e. transmission vs mortality) from the ecology notes has had much traction with virologists.


text:
DNA extraction from parasitic worm
I have a part of a parasitic worm frozen at -20°C. Do you think that DNA extraction using DNeasy kit without any pre-treatment is sufficient for DNA extraction?
Or would you recommend bead beating / nitrogen?
I do not need high quality DNA. It is just for the identification via shotgun metagenomics (shotgun metagenomics because 1) the parasite identification failed so far via PCR/immunostaining and 2) there is some human traces as well).
I refer to " DNeasy Blood & Tissue". It comes with protocols for eucaryotic tissue. The sample is extracted from ejaculate. I also do not need a whole lot of DNA, about 100ng should be enough.


text:
Why didn't Escobar's hippos introduced in a single event die out due to inbreeding
Today I read a BBC Report about how Pablo Escobar had once imported 4 hippos (1 male, 3 female) into his estate in Colombia for his private zoo. After his downfall, while other species were shipped out, hippos were considered too big to move and expected to not survive.
However, to the surprise of all the hippos are thriving and are so numerous that there have been calls to cull them. From the report:

Numbers are projected to only get bigger. [Colombian biologist Nataly] Castelblanco and her
peers say the population will reach over 1,400 specimens as early as
2034 without a cull - all of them descended from the original group of
a male and three females. In the study, they envisaged an ideal
scenario in which 30 animals need to be culled or castrated every year
to stop that happening.

My understanding is that since there was only 1 male, the gene pool would be limited and lead to lot of inbreeding in the descendants. This would cause population to not explode because some individuals would be unfit to survive.
Why has this not happened in case of hippos? Is it because there are 3 females (probably unrelated to each other) which keeps gene pool large enough? Or can mutations explain this phenomenon? Would results have been different if originally 2 females had been moved and only 1 retained?
EDIT - I have just found that current population is maybe less than 100 individuals which though big is not massive.
EDIT2 - I have edited the question title to keep focus on the hippos although a general answer would be welcome.

It is definitely not the case of all invasive species but in sunflowers at least, there is a tendency of invasive lineages to reproduce clonally (Bock et al, 2018)

It happens in other species.  Hamsters, for example.  Every golden hamster alive today is descended from 1 mother and a litter found in Syria in the 1930's, and there's millions (maybe billions?) of them due to their popularity as pets.  And hamsters don't live nearly as long as hippos, so we're talking far more generations, and a longer timespan, and that genetic bottleneck hasn't been a problem yet.

Keep in mind, it usually takes several generations for inbreeding to show its effects. The first couple of generations won't be that inbred at all, but as the inbreeding coefficient rises and the average individual is more and more related to one another they are more likely to show ill effects. Hippos only reach sexual maturity at about age five to six so there have only been a handful of generations born in Colombia as of now.

@DarrelHoffman at least according to wikipedia, that's not quite true about golden hamsters - only domestic ones (maybe only north american? wording unclear) and it also has a glaring "citation needed"

@llama Well, domestic hamsters are by far the majority of them - apparently a few have been found in the wild since, but nowhere near the numbers of domestic ones.  Either way, even if it is only North America, we're still talking about millions of hamsters descended from one litter.

The European royal families handily demonstrate that inbreeding isn't necessarily a showstopper.

I think one of the important things to understand in thinking about this case is that it just hasn't been that long, generationally.
Escobar imported the hippos in the late 1980s. Hippos reach sexual maturity at an average of about 7.5 years old for males and 9.5 years for females, space births about 2 years apart, and live for 40-50 years.  Thirty years out, this means that only about 3 generations have passed for females. Moreover, the dominant males are highly territorial, which means that much of the breeding might even now be still coming from the initial male and not his descendants. Still, the initial male breeding with his own daughters would indeed produce a significant inbreeding coefficient.
The impact of inbreeding, however, is also affected by the density of deleterious alleles. In geographically restricted species, the higher natural level of inbreeding can result in purging selection that leads to a much lower frequency of accumulated deleterious alleles than in highly social and gregarious species like humans and dogs. Hippos appear likely to be such a species, as well as having overall lower genetic variation than other large African mammals, suggesting a fairly recent expansion.
In short: it hasn't been that many generations, and if the inbreeding sensitivity of hippos is indeed fairly low to begin with, it may indeed be that there simply isn't any significant impact from inbreeding at this point in time.

Its also important to understand inbreeding does not guarantee a die out, it increases the chances of it. Its like being a heavy smoker makes lung cancer much more likely but does not guarantee you will get lung cancer.

Note that at least according to the BBC report "Indeed, conditions in their South American home seem so ideal for the hippos that studies show they start reproducing at earlier ages, she said." where "she" refers to Nataly Castelblanco - co-author of the article referenced in MikeSerfas' answer.  So they may well be beyond the 3 generations suggested in this answer.

They often do. You hear a lot about all of the times invasive species succeed in invading a new habitat, because there is a surviving population around for researchers to observe. There are lots of cases where new species are introduced to an environment in a single event but fail to survive. Rabbits and foxes were repeatedly introduced to Australia, only for most of the events to fail. The fact that there are rabbits and foxes there now is a consequence of the sheer number of times Europeans tried to introduce them. There are also many cases where captive animals escape captivity but fail to establish a breeding population, everything from "alien" big cats to coatimundis in Oklahoma.
This has actually been suggested to be one reason you don't see a lot of carnivores on islands. Carnivores might be able to disperse to islands, but they do so infrequently and the islands can't support their population that they end up dying out and we never know there was a dispersal event in the first place.
It's worth mentioning as well that many invasive species events probably aren't a "Noah's ark" type situation where you have only a couple of surviving adults. Many of the fishes that invaded the Great Lakes either did so in large numbers through the Welland Canal or were introduced in large number as eggs (smelt, salmon, some suspect alewives could have been introduced this way). Ballast ships can contain thousands of genetically distinct larvae and propagules of algae, small fishes, and invertebrates. Most deliberate introductions (e.g., rabbits and foxes in Australia) usually try to introduce enough individuals that inbreeding won't be a problem. Many invasive plants or feral domesticates (Asian carp, wild boar) were bred in captivity in large numbers and merely became wild.

The links you have posted are interesting! If I understood correctly, the second and third paras of the answer deal with overpopulation and multiple introduction events. As the question is specifically about dying out due to inbreeding (not over population) and from a small gene pool (rather than multiple individuals), maybe you would like to tackle those aspects as well?

I have edited the question title to make it clear that I am more interested in why the hippos thrived.

This is answering the opposite question. The question presumes that they should have died out like the examples you give, and asks why they didn't.

I'm almost tempted to purchase the rabbit article (just not $35 worth of tempted), as I was under the impression that a single release was the source of mainland rabbits.

@Barmar It's survivorship bias at work. Most of the introductions do fail, but we pay attention to the few that do succeed due to blind chance because they have a big impact on the local ecology. Thinking they represent the rule rather than the exception is the issue.

I don't think he's thinking they represent the rule, he seems surprised about it. And he's wondering how they achieved this miracle.

There are some references on this: Castelblanco-Martinez, 2021 is a recent one.  There doesn't seem to be much doubt at least that hippopotami are thriving as an invasive species.
I didn't see anything on the genetics, but I will give in to the temptation to speculate even if perhaps I shouldn't.  There are some advantages that are likely working against the effect of inbreeding depression:

being an invasive species with perhaps fewer diseases and predators or more assured access to resources that in their native range.
artificial selection to avoid deleterious alleles, if particularly healthy specimens were chosen for transport to South America by people who really did not want to leave their customer dissatisfied.
outbreeding enhancement ("hybrid vigor"), perhaps, if the founders were brought in from widely separated populations as a collector might tend to prefer.  Since we care about genetic diversity, not the literal number of founders (nor their sex, much) this directly opposes the bottleneck circumstance.
mundane issues: perhaps the females were imported pregnant, or an escaped hippo was surreptitiously replaced by a terrified lieutenant at his own expense.

Given these advantages, the hippos might do at least as well as the wisent, which was already facing extinction (suggesting harsher circumstances) before being reduced to 12 individuals, but has since begun to recover.

To focus on the inbreeding:

Inbreeding in itself is not a factor that would make species die out. Rather, inbreeding increases the risk of genetic diseases, if the deleterious alleles are already present.
Three females do not represent such a large genetic pool, so that inbreeding would still occur.
Given that there have been only few generations since the introduction event, there were obviously no outright deleterious alleles present, while it is too early to talk about dicrease in overall fitness.
Restoration of populations of nearly extinct species from small populations has been the focus of the conservation movement for over several decades. In many of the cases where a species was brought back to life we are talking about severely inbred populations. Notably, the modern population of Przhevalski's horses is claimed to descent from one ancestor.

Animals don't die out from any causes related to themselves, their breeding, or anything like that.  They die out either because their ecological niche goes away (climate change, etc.), because something else outcompetes them in that ecological niche (introduced fish outcompeting cichlids, for example), or because an external force exterminates them (dinosaurs and a damn great rock).
Inbreeding doesn't stop breeding - it just means they're more prone to certain developmental problems.  If you look at pure-breed dogs for example, all breeds are inbred because that's the very definition of a "pure-breed".  The result is that they're all very prone to issues with joints, eyes, arthritis, and more obscure issues like "cocker spaniel rage syndrome" (yes, that's a real thing).  None of this stops dogs from breeding though.
In the case of the hippos, they've been dropped into an ecological niche which is perfect for them, and which has no predators capable of limiting their numbers.  If given time and limited to that area, their numbers will naturally become limited by overgrazing and starvation.  But before that, they'll have made a complete mess of an environment which hasn't evolved to deal with hippos in it. Of course inbreeding means they'll develop some genetic issues which cause many individuals to be unhealthy in various ways, but it won't stop the herd from continuing.

Some individuals being unfit to survive, doesn’t necessarily lead to extinction, it leads to removing the traits that make them unfit to survive from the breeding pool.  From a species POV this is a good thing.
This leading to extinction happens when so many individuals have the trait, that those without it can’t can’t find a breeding partner to have children that don’t have the trait.
Critical in that happening is the trait being present in the breeding pool AND it making them unfit in the their current environment.  For instance, a trait that made them unfit to face off against lions or hyenas wouldn’t matter, if they aren’t fighting something that is at least similar to them.
Take snakes in Guam, lots of them probably came from similar small lots, but without predators, it doesn’t have so much of an immediate impact.  Of course that doesn’t mean they will be successful in the long term either, as they are likely to run out of prey and starve to death.


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In CRISPR bacteria, how does viral genomes get integrated into the spacers of CRISPR? Also, in its use, where does Cas9 cut the DNA?
I've been out of Biology for about a year polishing my programming skills. I know CRISPR/Cas9 allows targeted 'cutting' of DNA via RNA-guidance. Few questions regarding this.

Regarding to its natural phenomenon, when a virus infects a microbe with CRISPR capabilities, how does the genome get integrated into the 'spacers' of CRISPR region versus elsewhere of the prokaryote genome so that when transcribed, the Cas enzymes know that it's a foreign DNA element to be targeted? My understanding of virus infections is a little cloudy too; I'm thinking random transpositions.
I'm looking into it now, so I may figure this out before someone answers, but when the target DNA is located via the guiding RNA, where does the Cas9 enzyme decide to 'cut' -- rendering it useless -- the DNA, and how does it identify the location?

-EDIT- Ah. The target sequence must also include a 'PAM' sequence downstream (Protospacer Adjacent Motif), which allows binding of the riboprotein complex(guiding RNA + Cas9), and biochemistry magic cuts it ~3-4 bases upstream of the PAM). citation: https://www.addgene.org/CRISPR/guide/

Just thought of another question, if the DNA is cut at the seemingly specific spot, is the DNA repair that ensues downstream totally random? I feel like it would be in the organism's best interest (anthropomorphogenic, oops), and evolution generally says it usually does, to have a mechanism to repair it to its original state.

Right on, me too, this an amazing technique that i would like to know more about.

This paper should clear up a lot more than anyone on here truly can about the CRISPR system.
CRISPR/Cas9 is very unique, even compared to other proteins purified from bacteria like Taq Poly.

The reason is due to how complex it is actually induce this protein. Essentially you are transfecting a plasmid with the Cas9 protein and its guide RNA (gRNA) on the vector. Transfecting itself is not easy, not to mention you are essentially adding a mechanism to a cell trying to knockout genes and you've got a handful. In fact doing that for one cell line, and noting the effects of what you knocked out, would be enough to produce a paper in a pretty impactful journal. (Image from: https://www.systembio.com/)
Also some recent advancements in CRISPR include:

Light-induced CRIPSR/Cas9 (easier regulation of enzymatic activity)

Basically these researchers were trying to deduce a method allowing for more control of the CRISPR technique, since CRISPR has had issues with off-target effects. While it isn't a change in how CRISPR works, or even where, the change is how much you can control the reaction. Simply put they devised a way that allows you to turn CRISPR on/off using light allowing more precise control of its activity. Surely it will be helpful to reduce off target effects.
"This was accomplished by fusing the light-inducible heterodimerizing proteins CRY2 and CIB1 to a transactivation domain and the catalytically inactive dCas9, respectively." (Lauren R Polstein & Charles A Gersbach)

Cpf1 to replace Cas9 as cutting protein (more percise activity)

This one is a bit more interesting in that it is a direct change to the CRISPR system itself. Cas9 has been the standard cutting protein used for the CRISPR system although it has had controversy due to its somewhat imprecise cutting. Cpf1 has been shown to be more precise (so their data says) and it is now being implemented by some to see if this is truly the case. Combined with the above "light-induced" system this brings CRISPR down to safer levels when talking about off-target effects.
Here are some good online seminars to get you started:

CRISPR/Cas9 from start to finish
Improve CRISPR-Cas9 experiments with rationally designed guide RNAs

These seminars I can't really comment directly on because they explain everything so well on their own. Anything I say really will only detract from what they are teaching since I am by no means an expert with CRISPR but simply someone who is looking into possibly using it for my lab. Right now there is a lot of guide material on how to properly format your CRISPR experiments but my personal opinion is to give the technique maybe a year or two more when it is more standard for research.
That is unless you want to directly research the method and improve it in your own way.
Let me know if this answers your questions sufficiently.
Sorry that I cannot do much more in terms of explaining the links. The studies are not ones I can easily access unless I am at work since I usually access them through the university.
As far as the repair mechanism goes (your #3 question) I can't really answer that for sure but I have recently received a pamphlet that describes how to ensure the cells uses HJ rather than NHEJ.

This is a link-only answer, which are discouraged on StackExchange. Could you describe what is in these links and include relevant areas of the text?

I added some more of my own words. I'm afraid I was a bit hesitant to really say much more since I am not much of an expert.


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Spatial dimensions for an animal
I'm reading a review paper. They say:

The position of an object in head-centered coordinates (that is, relative to an animal's head) can be defined along three axes: the medio-lateral (radial) axis, the rostro-caudal (horizontal) axis and the dorso-central (vertical) axis.

I'm having a little bit of difficulty understanding this coordinate system as the paper doesn't provide a picture. Usually I would think of the three axis as an x-y-z coordinate system where the rat's head is the "origin" (from a mathematical standpoint), but the terminology here seems to be a bit different, so I'd like to understand from a biologist's point-of-view how these three axes are drawn relative from a rat's head.
Paper can be found here: http://www.nature.com/nrn/journal/v9/n8/full/nrn2411.html (bottom of page 602)

@Remi.b Thank you for the edits and I have included a link to the paper.

Rereading the quote, I realize that in parenthesis, the common meaning of the three axes are indicated. Are the terms "radial", "horizontal" and "vertical" unclear to you in this context?

@Remi Yes they are unclear, specifically they're unclear to me what they referring to relative to a rat's head (e.g. is horizontal axis from the rat's head through it's body, or is it perpendicular to the body through the head? If it's the latter, then what is the axis through the rat's body called?, etc.)

Wikipedia has a quite didactic article on this: https://en.wikipedia.org/wiki/Anatomical_terms_of_location#Axes
These terms are complementary with a mathematical coordinate system: if you are describing a system of axis for a cylinder, you will need to specify that (e.g.) $z$ is along its symmetry axis, here you will say that $z$ is along the rostro-caudal (or antero-posterior) axis. Also, in biology, axes do not have to be straight lines, see the neuraxis:

The so called horizontal axis (rosto-caudal) is parallel to the body of the rat.  Vertical is just vertical when the rat is in its normal standing position and medio-lateral is horizonral and perpendicular to the rat's body. The head is the origin.


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Head transplant feasibility - Project HEAVEN-GEMINI
There is a news circulating that in the next two years, Dr. Sergio Canavero, of the Turin Advanced Neuromodulation Group (TANG) in Italy, will perform the world's first head transplantation. A procedure which will require

150 surgeons and nurses approximately 36 hours to complete

and after which the patient is held in coma during recovery

The recipient will be kept in a coma for around 3-4 weeks, says Dr. Canavero, during which time the spinal cord will be subject to electrical stimulation via implanted electrodes in order to boost the new nerve connections.

Is this even feasible? If it can be done, does that imply that humans can live for a long time, if they can find a compatible donor ? What requirements are there for compatibility?

I have the impression that the MNT article is significantly over-stating the potential of this technique, at least with current technology. The mouse work by Xiaoping Ren (see this 2014 paper) seems to have a very steep death-curve post-surgery:

Forty Kunming mice and forty C57 wild type underwent the
  AHBR  procedure.  After  transplantation,  18  mice  survived
  for 3 h after the ventilator was disconnected.

There are no details in the paper about how long the most robust mouse survived for post-surgery. I would guess that it is not an impressive number, otherwise the authors would include it. Alternatively, the 18 surviving mice may have been euthanased after three hours - the paper does not make this clear, but it is common to have a predetermined time-limit for euthanasia in experiments where animals are expected to suffer from an irreversible treatment.

During these 3 h, the mice
  awakened and displayed normal cranial nerve function and
  characteristic responsiveness (blinking, whiskers moving, etc.).
  After the mice awoke, electroencephalogram (EEG) recordings
  were  made  directly  from  the  cortex  of  the  transplanted
  Cephalons (Figure 3). Because blood supply was maintained at
  an adequate level during surgery by anastomosing the donor
  and recipient carotid and jugular vessels, the intra- and post-
  operative EEG and ECG show electrophysiological activity.

This sounds a lot like a 'no' to 'can this technique be used to substantially extend human lifespans?', on current technology. If a human trial is approved, and is as successful as the mouse trials, the recipient will likely be dead within hours. If they survive for several hours, the level of motor control that can be expected in that time is likely restricted to unconscious motor tics (cf whisker twitching and blinking).


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Is the skin of feline jungle predators protected against ants?
I was watching a video of a jaguar stalking along a riverbank, killing prey, climbing up the muddy bank, then laying in thick brush to eat. My first thought about this is that there must be tons of ants. I've never been to a jungle but on muddy river banks around where I live if you crawled around near the water and on the forest floor in general you'd be sure to get attacked by ants and it would result in hundreds of bites which cause swelling, major discomfort, and perhaps infection.
This seems like it would be a problem for large mammal jungle predators that kill prey in that kind of river bank area and then plop down and eat it. Does the fur make them immune to ant bites, or ants more rare in the jungle than I imagine, or they do get bitten but they just have a high tolerance for pain?


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Why is sexual reproduction so much more common than asexual (in macroscopic organisms)? Fundamentally, what makes it better?
I'm experimenting with an evolutionary method of creating a neural network. I use an asexual approach, but I've seen others use sexual approaches.
So I'm interesting in learning what's better about sexual reproduction as apposed to asexual, and biology is probably the best way to approach that question. So, why is sexual reproduction so much more common than asexual (in macroscopic organisms)? Fundamentally, what makes it better?
I'm struggling to understand what the combination of two gene sets does that couldn't be achieved by mutations to a child of asexual reproduction.

I'm not so sure "more common" is true unless you are talking about particular types of life. There are many very successful organisms that reproduce primarily via asexual reproduction.

I edited to specify macroscopic

Genetic diversity is needed to prevent everyone from dying of the same disease. This is the problem with monocultures. Higher organisms are more susceptible to disease and thus reproduce sexually.
Furthermore, basically all organisms exchange DNA so they are effectively sexual.


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Is the strength of presynaptic stimulus on the postsynaptic neuron affected more by the dendrites, or the cell body?
Is the strength of presynaptic stimulus on the postsynaptic neuron affected more by the properties of the dendrites & axon terminals, or the cell body & axon?

Two years ago I asked a question here and learned that neurons do have a bias, and that various factors affect that bias, and now I'm trying to learn more specifically, how much of the strength of the the strength of a synapse, i.e. the size of the effect of a presynaptic stimulus on the postsynaptic neuron is dependent on the properties of each individual axon terminal / dendrite terminal, vs how much is dependent on the properties of the axon or cell body.
And do the properties of each individual axon terminal / dendrite ending vary diversely, even among dendrites of the same neuron, or do individual dendrites and axon terminals of the same neurons typically have similar properties?

I think this question is far too broad. You are better off thinking about what actually happens in neurons postsynaptically rather than trying to think in terms of what's "more important"  A or B - that sort of question isn't really answerable.

It depends on the type of axon, of course.
In Axosomatic synapses the properties of dendrite is not important, but for Axodendritic synapses, the properties of post syn. dendrite is more important as the amplification and other processing happen there. However, Soma is much nearer to Axon hillock, so changes by Soma wouldn't be declined as the impulses won't. It may be depended on neuron properties itself and so that's wrong to generalise!


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How does the brain avoid feedback loops?
The article Ants Swarm Like Brains Think really helped me to understand the way that neurons which are pretty dumb on their own (like ants) can work together to create a pretty genius system (a brain or an ant-hive). The idea is that both the neurons and the ants function majorly via positive and negative feedback, which is really neat to understand.
However as shown in that article, sometimes groups of ants get caught in something called a feedback loop. They can repeat the same action over and over because the positive feedback is just being relayed from ant to ant to ant in a circle, and the ants can do something unhealthy such as walk in a circle for days. I don't know any examples of negative feedback loops but they would presumably also be unhealthy.
As noted in the comments, this is an analogy, but not without a good reason: The brain does work via positive and negative feedback. And that does create the potential for feedback loops.
So I'm curious about what biological features in neurons help to avoid these feedback loops in our brains. How does the brain avoid feedback loops?

The article is cool, but it's using an analogy. The brain doesn't really work, strickly speaking, as an ant swarm.

@Tivie of course, but the analogy is not without a good reason: The brain does work via positive and negative feedback. And that does create the potential for feedback loops.

Well, sometimes, it does enter a kind of feedback loop, Epilepsy.

@Tivie very true. So I'm even more curious now, about how most brains avoid them. Of course, Epilepsy may be far more complex than feedback loops, but it could be a good example of one.

I will try to post a simple answer

well balanced feedback loops create oscillations as well...

@jt0dd This is interesting. I just realized that feedback loop is not a common network motif in neural networks. Feed-forwards/bi-fan are very common. There should be a reason for this: something theoretical. I shall post when I get an answer to this

@WYSIWYG neat please explain

@jt0dd I was referring to the architecture of neural networks. I will have to look up for the reason to why FF is more common than FB

@jt0dd. I can think of a few reasons why FB is not preferred. It would take a long time to generate a FB. Therefore is is best to anticipate the fluctuation beforehand and correct/fix it.

Normally, after an excitatory neuron fires, it becomes more resistant to firing again for a period of time (refractory period). This is due to electrical changes within the excitatory neuron.
After depolarazing and reaching an action potential(firing), the neuron enters the refractory period, in which its charge will go back to normal (resting potential). This refractory period can be divided in two phases: Absolute and relative. During the Absolute refractory period, the neuron cannot be discharged again, since the sodium channels are inactive.
It's the relative refractory phase, however, that is more relevant to your question. During this period, the neuron enters a hyperpolarization states, meaning that it's resistant to firing again, unless it receives a greater stimulus.
So, basically, after firing and for a while, a neuron requires greater stimulus to be fired again. This works as a Feedback control, since even if you overstimulate a neuron it can fire only so often.
Inhibitory and excitatory neurons (and inhibitory and excitatory neurotransmitters) also play a role in the feedback control. Inhibitory neurons reduce the likelihood of a postsynaptic neuron to fire while excitatory neurons do the opposite.

However, sometimes these mechanism fail.
For instance, in Epilepsy, the resistance of excitatory neurons to fire during the refractory period is decreased. A group of neurons begin firing in an abnormal, excessive, and synchronized manner, resulting in a wave of depolarization known as a paroxysmal depolarizing shift, causing seizures.
In Parkinson disease, decreased dopamine causes increased inhibitory output (excess negative feedback) of the motor circuit, which leads to hypokinesia.
In contrast, excess dopamine and dopaminergic neuron activity seem to be related with Schizophrenia.

thank you for this explanation. Do you happen to know the relative timespan of neuron-neuron signal propagation and the refractory period? In other words, how many neurons would need to be in a positive feedback loop to moot the refractory effect. And is this much longer than a normal signal path?

@FullDecent has a great followup question here. Say the refractory period is 250ms. Then there could be a feedback loop as long as the time the signal takes to return to the starting node is at least 250ms.


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Why are Birds and Reptiles with abundant yolk sac polyspermic?
I was given an explanation that birds and reptiles are polyspermic because they have an abundant yolk sac. But how does it explain the thing?
Chicken as an adult is not using in my opinion yolk as an energy source.
Yolk is used during embryogenesis as the primary energy source with blastula and gastrula -stages and during organogenesis, since the embryo needs proteins and energy somewhere.
How does abundant yolk sac make birds and reptiles polyspermic?

My professor says that

The yolk sac is not connected to the mechanism of polyspermy or
  monospermy. [Amount of yolk inside the oocyte is then again.]  The
  oocytes of reptiles and birds are yolk rich  - polylecithal  for instance.

where
lecithal = yolk containing and some pieces of information about here.


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Is this mammalian embryo blastocyst, gastrula or only phase between them?
The picture shows the formation of early blastocyst and late blastocyst.
The middle embryo has embryoblast.
My professor says that blastocyst in general has embryoblast and trophoblast.

Embryoblast is the inner cell mass but the thing has none of it.
The last embryo does not seem to have inner cell mass anymore.
Is the last embryo in the picture anymore blastocyst?
The given thing seems to be "the single layered blastocyst that will give rise to gastrula", Wikipedia Gastrulation. The given stage seems to last very short time. It probably should be called phase between blastocyst and gastrula so that the thing is not blastocyst and not gastrula.
What is the right name for the given thing in mammalians?

Again, the thing (2) is idealized and probably does exists at all. It is an idealized picture. It is really a mistake to call such a thing blastocyst like Wikipedia does. The thing should be fixed not to confuse other people.
There should be real pictures instead of such idealized ones.

At undergraduate level you should not rely on Wikipedia. Good textbooks and journal articles are much better sources.

Completely true. Wikipedia has confused me a lot. I will rely on textbooks now on. I just love my Gilbert's textbook and Albert's biology book. They explain things so that I understand it.


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What is a good review article source for Physiology?
I am looking review articles for Physiology.
For instance, Physiological explanation of steps of measurement of the metabolism by Douglas-Haldane.
There is no section for Physiology or metabolism in Advanced Search of Nature Review.
What is a good review article source of Physiology?

Annual Review of Physiology? http://www.annualreviews.org/journal/physiol However the Douglas-Haldane method was published in 1913, so I'm not clear what you are hoping to find in recent reviews, but then again its really not my field.

The Journal of Physiology
Annual Reviews Physiology
Journals from American Physiological Society
Frontiers in Physiology
Experimental Physiology
Often, notable research papers are published in journals with high impact factors, although being published in a journal with high impact factor does not mean the research is better over research in smaller journals. But it can be a rough indication.